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Infectious Disease > Week 4: Sexually Transmitted Infections > Flashcards

Week 4: Sexually Transmitted Infections Flashcards

1
Q

Question

A

C. They don’t survive long without warmth and moisture

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2
Q

Features of sexually transmitted diseases

A
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3
Q

Epidemiology of STDs

A
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4
Q

Most common STD

A

Chlamydia

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5
Q

Why are STDs prevalence increasing

A

?

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6
Q

Chlamydia clinical manifestations

8 listed

A
  • Urethritis
  • Cervicitis
  • PID
  • Epididymitis
  • Proctitis
  • Conjunctivitis, Trachoma
  • Neonatal pneumonia and conjunctivitis
  • Reactive arthritis
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7
Q

Gonorrhea clinical manifestations

8 listed

A
  • Urethritis
  • Cervicitis
  • PID
  • Epididymitis
  • Proctitis
  • Conjunctivitis
  • Neonatal conjunctivitis
  • Disseminated infection
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8
Q

Why are the clinical manifestations of Chlamydia and Gonorrhea similar?

A

They both adhere to columnar epithelium

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9
Q

What is Urethritis?

A
  • infection of urethra (not urinary tract infection)
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10
Q

Gonococcal urethritis or cervicitis incubation period

A

3 - 7 days

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11
Q

Urethritis signs & symptoms

A
  • dysuria
  • purulent discharge
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12
Q

Cervicitis signs and symptoms

A
  • Dysuria (pain with urination)
  • Purulent discharge
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13
Q

Gonococcal urethritis and cervicitis

A
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14
Q

Gonorrhea pathogen

A

Neisseria gonorrheae

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15
Q

Neisseria gonorrheae classification

A

Gram-negative diplococci (not truly intracellular)

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16
Q

Neisseria gonorrheae tropism

A

Adhere to columnar epithelium

  • Cervix
  • Urethra
  • Rectum
  • Eye
  • Throat
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17
Q

Neisseria gonorrheae discharge

A

Vigorously purulent response

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18
Q

Neisseria gonorrheae immune response

A
  • Vigorous purulent discharge
  • Phagocytosed by WBCs
  • Pili are antigenically variable
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19
Q

Examples of diplococci

A
  • Neisseria gonorrheae
  • Neisseria meningitidis
  • Moraxella sp
  • etc.
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20
Q

Gram-stain of Neisseria gonorrheae

A

gram-negative diplococci (pink)

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21
Q

How is gonorrhea diagnosed?

A
  • Gram stain - gram-negative diplococci
  • Culture media chocolate agar in high-CO2 atmosphere
  • Nucleic acid amplification
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22
Q

Gonorrhea culture details

A

Chocolate agar in high CO2 atmosphere

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23
Q

Gonorrhea nucleic acid amplification from where?

A
  • Urethra
  • Cervix
  • Throat
  • Rectal
  • Urine
  • Vaginal
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24
Q

Gonorrhea evolution of resistance

A
  • has acquired multiple plasmid and chromosomal resistance mutations
  • Becoming resistant to a lot of conventional antibiotics
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25
Q

Resistance tracking of Neisseria gonorrheae

A
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26
Q

First-line treatment for gonorrhea

A

Ceftriaxone

or

Cefixime

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27
Q

Neisseria gonorrheae susceptibility patterns

A
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28
Q

Recommended treatment for Gonorrhea

A

Ceftriaxone and Azithromycin

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29
Q

Ceftriaxone method of use

A

IM

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30
Q

Ceftriaxone drug class

A

3rd generation cefalosporin

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31
Q

Considerations of gonorrhea treatment

6 listed

A
  • Be sure the patient is treated correctly
  • Be sure the partner is treated
  • All abstain from sex for 7 days
  • Report case to DOH
  • Educate patient
  • Promote development of new drugs
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32
Q

Question

A

D. the surface antigens mutate frequently (surface pili proteins are antigenically variable)

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33
Q

Chlamydia pathogen

A

Chlamydia trachomatis

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34
Q

Chlamydia trachomatis classification

A

Obligate intracellular bacterium

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35
Q

Chlamydia trachomatis tropism

A

Adhere to columnar epithelium cells

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36
Q

Chlamydia trachomatis gram stain

A

Outr membrane is like gram-negative bacteria but does NOT gram stain

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37
Q

Chlamydia trachomatis features of intracellular infection

A
  • Doesn’t make its own ATP so it uses host cell ATP
  • Cytopathic effect: cytoplasmic inclusion bodies
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38
Q

Chlamydia trachomatis culture

A

Culture requires Eukaryotic cell line so they are rarely done

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39
Q

Memory immune response and Chlamydia trachomatis

A

Immunity does not protect against reinfection

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40
Q

Describe the life cycle of Chlamydia trachomatis

A

Slower life-cycle so it requires a longer duration of anti-biotic

Have 2 different forms

Start out as Elementary bodies (more hardy survive in the environment) where they stick on columnar epithelial cell and enter the cell and form Reticulate bodies and replicate and form inclusion bodies and continue replicating until cell lysis and release of more chlamydia in the Elementary body form to infect more cells

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41
Q

Chlamydia and gonorrhea are most common in what age group?

A
  • young people
  • more common in women
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42
Q

Chlamydial urethritis incubation

A

7 - 21 days

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43
Q

Chlamydial urethritis signs & symptoms

A
  • Dysuria (pain while urinating)
  • A discharge which is often clear or scant
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44
Q

Chlamydial urethritis gram stain

A

white cells, no organisms seen

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45
Q

Chlamydial urethritis vs Gonorrhea urethritis

A

Gonorrhea is often more inflammatory and produces a purulent discharge while Chlamydia is less inflammatory and produces a clear or scant discharge

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46
Q

Chlamydial Cervicitis incubation

A

7-21 days

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47
Q

Chlamydial Cervicitis signs & symptoms

A
  • Dysuria (pain while urinating)
  • A discharge which is often clear or scant
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48
Q

Chlamydial Cervicitis gram stain

A

white cells, no organisms

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49
Q

Chlamydial Cervicitis vs gonorrhea cervicitis

A

Gonorrhea is often more inflammatory and produces a purulent discharge while Chlamydia is often less inflammatory and produces a clear or scant discharge

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50
Q

Pictures of Chlamydial urethritis or Cervicitis

A
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51
Q

PID AKA

A

Pelvic inflammatory disease

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52
Q

PID caused by Chlamydia or Gonorrhea

A

Chlamydia and gonorrhea start in the cervix and can progress if not treated up to the uterus and fallopian tubes where there is also columnar epithelium and cause a lot of inflammation and adhesions which can cause infertility, chronic pelvic pain, ectopic pregnancies (fallopian tube damage)

53
Q

Complications of Chlamydia in women AND Gonorrhea

A
54
Q

What is the most common presentation of chlamydia?

A

Absolutely no symptoms

55
Q

How is Chlamydia diagnosed

A

Antigen detection methods

DNA probe

Nucleic acid amplification (NAAT)

56
Q

Tissue culture of Chlamydia

A
  • Expensive
  • insensitive
57
Q

Chlamydia Antigen Detection Methods

A

Insensitive

58
Q

Chlamydia DNA probe

A

more sensitive

59
Q

Test of choice for Chlamydia

A

NAAT (Nucleic Acid Amplification)

60
Q

Chlamydia NAAT

A
  • most sensitive

can do on

  • urine
  • anal swab
  • cervix
  • throat
  • self-collected
61
Q

Chlamydia screening parameters

A
62
Q

Chlamydia and pregnancy

A

Conjunctivitis and pneumonia in neonates

63
Q

Gonorrhea and pregnancy

A

Conjunctivitis

64
Q

When is Chlamydia and Gonorrhea transmitted during pregnancy?

A

Transmitted at the time of delivery

65
Q

Pregnant women and STD screening

A

SCREEN ALL PREGNANT WOMEN!

66
Q

Chlamydia treatment

A

want something that gets into cells and has a long half-life

(Tetracycline, newer Doxycyline)

Azithromycin

67
Q

Unique syndromes associated with Gonorrhea

A
  • Disseminated gonococcal infection
    • Bacteremia
    • Skin Pustules
    • Septic Arthritis
    • Tenosynovitis
68
Q

Unique syndromes associated with Chlamydia

A

Reactive arthritis

  • arthritis
  • Skin lesions
  • Dysuria
  • Eye problems
69
Q

Differential Diagnoses of Genital ulcers

A

STIs

  • Herpes Simplex
  • Syphilis (Treponema pallidum)
  • Chancroid (Hemophilus ducreyi)

Autoimmune

  • Behcet’s
  • Reactive arthritis (circinate balanitis)

Drug toxicity

  • Fixed drug eruption

Other infectious and non-infectious conditions

70
Q

Herpes Simplex Virus classification

A

Enveloped, double-stranded DNA virus (susceptible to soap and water (lipid envelope))

71
Q

Type 1 Herpes Simplex virus

A

Usually oral

72
Q

Type 2 Herpes Simplex virus

A

usually genital

73
Q

Prevalence of HSV-2

A
  • 17% of US adults
  • Most who have it don’t know they have it
74
Q

Herpes simplex virus duration of infection

A

Latent in neurons, reactivates periodically with or without symptoms

Herpes is forever

75
Q

How can herpes simplex virus be transmitted?

A

can be transmitted from symptomatic sores or can even be transmitted by asymptomatic shedding

76
Q

Herpes simplex virus severity

A
  • Nuisance for most people giving them a couple of sores every couple of months
  • Can be serious in immunosuppressed or neonates - transmitted at time of delivery can be very bad or lethal (however neonatal herpes infections are very rare)
77
Q

Vaccine for Herpes

A

No vaccine yet

78
Q

Treatment of Herpes Simplex Virus

A
  • Acyclovir
  • Valacyclovir
  • Famciclovir

episodically for outbreaks or daily for suppression

79
Q

Pictures of Genital HSV

A
80
Q

Syphilis pathogen

A

Treponema pallidum

81
Q

Treponema pallidum causes

A

Syphilis

82
Q

Treponema pallidum family

A

Spirochete family

(others in family: Borrelia, Leptospira)

83
Q

Treponema pallidum classification

A
  • too small for light microscopy
84
Q

Treponema pallidum culture

A
  • Cannot grow in vitro
  • Can inoculate into mammals for research
85
Q

Diagnosis of Treponema pallidum

A

Direct visualization by special staining

Serology: Can be challenging to interpret

86
Q

Treponema pallidum treatment

A

curable with penicillin

87
Q

Syphilis prevalence

A

Was very common around 1900s but it is increasing again

88
Q

Syphilis serology

A
89
Q

Once you have had syphilis what antibody do you have

A

Always have Treponemal antibody if you’ve had syphilis

90
Q

Categories of syphilis serology tests

A
  • Nontreponemal (antibodies against self as a result of syphilis infection)
  • Treponemal
91
Q

Characteristics of nontreponemal syphilis serology

A
  • RPR, VDRL
  • Quantitative
  • Titers go down with treatment
  • False positives and negatives
92
Q

Characteristics of treponemal syphilis serology

A
  • TPPA, MHA-TP, FTA
  • Qualitative
  • Stays positive for life after an infection
  • More specific than nontreponemal
93
Q

False positives of nontreponemal Ab tests can be related to

A

other autoimmune antibodies causing a false positive for syphilis

94
Q

Rates of primary and secondary syphilis

A
95
Q

Describe the distribution of syphilis

A
96
Q

How does syphilis get into the body

A

The delicate spirochetes can enter the body if there is cracked skin or microabrasions, or if they get through columnar epithelium

97
Q

Events of syphilis infection

A
  • immediately after syphilis enters the body you will get an immune response causing a local ulceration (Chancre)
  • After that they can enter lymph nodes which can cause local lymphadenopathy but from the lymphatic system can distribute throughout the body
98
Q

Syphilis staging

A
  • Primary
  • Secondary
  • Latent
  • Tertiary
  • Neurosyphilis
  • Congenital syphilis
99
Q

When would a syphilis infection be staged as primary

A

2-3 weeks after infection

100
Q

When would a syphilis infection be staged as secondary

A

6-12 weeks

101
Q

When would a syphilis infection be staged as latent

A

where there is a positive blood test so the patient is infected but there are no current signs or symptoms

102
Q

When would a syphilis infection be staged as tertiary

A

sometime after 12 weeks

103
Q

Describe the signs and symptoms of primary syphilis

A
  • Chancre at entry site
  • regional lymphadenopathy
104
Q

what is this?

A

Chancre (syphilis)

105
Q

Serology of primary syphilis

A

serology may not yet be positive

106
Q

Signs & symptoms of secondary syphilis

A
  • Rash
  • joint pain
  • hepatitis
  • general lymphadenopathy
  • etc
107
Q

Signs & symptoms of latent syphilis

A

Positive blood test so patient is infected but there are no signs & symptoms

108
Q

Signs & symptoms of tertiary syphilis

A
  • CNS damage
  • Aorititis
  • gumma
  • other late sequelae
109
Q

When does neurosyphilis occur?

A

CNS infection can happen at ANY stage of syphilis

110
Q

How is congenital syphilis transmitted from mother to baby

A

Passed through the placenta

111
Q

Primary chancre

A

usually painless

112
Q

Rash of secondary syphilis

A

can be anywhere and can be highly variable but this rash can also go on the “palms and soles”

113
Q

Condyloma lata

A

secondary syphilis

114
Q

Patchy alopecia

A

secondary syphilis

115
Q

Mucous patches

A

Secondary syphilis

116
Q

Signs & symptoms of congenital syphilis

A
  • Miscarriage
  • Stillbirth

Early or Late

  • Hepatomegaly
  • Meningitis
  • Rash
  • CBC changes
  • Bone changes
  • Blindness
  • Deafness
  • CNS damage
117
Q

Most important thing to prevent congenital syphilis

A

Screen ALL pregnant women

118
Q

What is Vaginitis?

A
  • Vaginal discharge/discomfort
  • Not necessarily an “-itis” (inflammation)
119
Q

Common causes of Vaginitis

A
  • Bacterial vaginosis
  • Candida
  • Trichomonas
  • Many other infectious and non-infectious causes
120
Q

Normal vaginal flora

A

Lactobacillus and other good bacteria

121
Q

Epidemiology of HPV and genital worts

A

Prevalent (mostly asymptomatic)

122
Q

Signs & symptoms of HPV and genital worts

A
  • Mostly asymptomatic
  • Some strains more likely to cause warts (6, 11)
  • Some strains more likely to cause dysplasia (16 & 18 > 31, 33, 35, 52, 58)
  • Infection and warts may spontaneously resolve
  • Worse in immunocompromised
123
Q

HPV strains more likely to cause warts

A

6 & 11

124
Q

HPV strains more likely to cause dysplasia

A

16 & 18 > 45, 31, 33, 35, 52, and 58

125
Q

HPV tropism

A

Only infects squamous epithelial cells

126
Q

Pathology of HPV

A

Viral E6 and E7 proteins immortalize squamous cells -> cervical, anal, head/neck squamous cancer

127
Q

Treatment of HPV

A
  • No antiviral medication
  • Vaccine greatly reduces warts and dysplasia
  • The vaccine effective against multiple strains
128
Q

Prevalence of cervical dysplasia

A
129
Q

Principles of STI management

A
  • Evaluate patient for other STIs, including HIV
  • Evaluate and treat all recent partners
  • Educate patient: treatment failure, reinfection, prevention
  • Condoms reduce risk
  • Notify public health department (reportable diseases)
  • Follow CDC treatment guidelines

Infectious Disease (82 decks)

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