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MIC3041 Medical Microbiology > Sexually Transmitted Infections > Flashcards

Sexually Transmitted Infections Flashcards

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1
Q

How many new STIs each year?

A

~500 million

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2
Q

What are the 6 factors for why STIs cause such a burden of disease?

A
  1. Often asymptomatic
  2. Stigma about getting tested/unaware
  3. Often incurable/long term infections
  4. Lack of education/disempowerment
  5. People unwilling to change behaviour/behaviours private
  6. People like having sex
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3
Q

What are 2 important considerations to have towards STIs?

A

Generally fragile organisms involved
- survive poorly outside of the body
- transmission requires close contact and/or direct transmission of bodily fluids
May have multiple infections at once
- one infection may increase susceptibility to other infections

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4
Q

If you have one STI already how does that impact the ability of transmission of HIV?

A

HIV transmission increases by 5-10 times

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5
Q

What are the 6 most common bacterial causes of STIs?

A 
Chlamydia trachomatis
Neisseria gonorrhoea
Treponema pallidum
Haemophilus ducreyi
Mycoplasma genitalium
Gardnerella vaginalis
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6
Q

What are the 4 most common viral causes of STIs?

A

HIV
HSP
HPV
HBV

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7
Q

What is the most common fungal cause of STIs?

A

Candida albicans

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8
Q

What is most common protozoan cause of STIs?

A

Trichomonas vaginalis

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9
Q

Describe cervicitis and urethritis

A

Inflammation of cervix and urethra

Symptoms: dysuria, itching, +/- discharge

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10
Q

Which organisms cause cervicitis and urethritis?

A

N. gonorrhoea
C. trachomatis
M. genitalium
HSV

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11
Q

Describe vaginosis

A

Disrupted vaginal flora

Symptoms: unpleasant odour and/or vaginal discharge

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12
Q

Which organisms cause vaginosis?

A

T. vaginalis
C. albicans
G. vaginalis

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13
Q

Which organisms cause genital ulcers?

A

HSV
C. trachomatis
T. pallidum
H. ducreyi

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14
Q

Describe pelvic inflammatory disease

A

Symptoms: chronic pelvic pain, fallopian tube damage, infertility

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15
Q

Which organisms cause pelvic inflammatory disease?

A

C. trachomatis
N. gonorrhoea
G. vaginalis
Mycoplasma hominis

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16
Q

Effects of HIV

A

> 40 million people infected

~1 million deaths/year

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17
Q

Effects of HSV

A

> 500 million people infected

~20 million new infections/year

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18
Q

Effects of HPV

A

~30 million infections/year

~250,000 cancer deaths/year

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19
Q

Effects of HBV

A

> 200 million people infected

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20
Q

Describe HIV

A

HIV-1 and HIV-2
Retrovirus of the lentivirus family
Encode a reverse transcriptase (pol gene)

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21
Q

What is HIV the causative agent of?

A

Acquired Immune Deficiency Syndrome (AIDS)

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22
Q

What does HIV infect?

A

CD4+ cells

  • T helper cells, monocytes
  • Dendritic cells
  • Microglia
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23
Q

How is HIV transmitted?

A 
Transmitted in body fluids
Non-sexual
- blood
- mother to child (vertical transmission)
Sexual
- male to male
- male to female
- female to male
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24
Q

What is the most common transmission of HIV in Africa and Asia?

A

Female to male transmission

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25
Q

Describe HIV pathogenesis

A 
Initial acute phase:
- Massive loss of CD4+ T cells
-> profoundly weakens the immune system
- Stage lasts for a few weeks
Second chronic phase:
- HIV replication checked by immune system
-> chronic immune activation
-> increasing threat of opportunistic infection
- Stage lasts for several years
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26
Q

Describe AIDS onset

A

A wide array of disease associated with HIV-induced immune compromise
Infections often in unusual tissues

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27
Q

How is HIV treated?

A

Treated with drugs that mostly target the reverse transcriptase step of HIV replication
- Nucleoside RT inhibitors (NRTIs)
- Non-nucleoside RT inhibitors (NNRTIs)
Also protease inhibitors and fusion inhibitors
Current use of combined therapy
- Highly active antiretroviral therapy (HAART)

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28
Q

Describe HSV

A

Caused by herpes simplex virus

Double-stranded DNA virus, large genome

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29
Q

Describe HSV-1

A

Generally transmitted by saliva
Oral cold sores ~70% seroprevalence in adults
Accounts for 50% of new genital herpes causes in developed countries

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30
Q

Describe HSV-2

A

Generally transmitted by sexual contact

Genital blisters/ulcers

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31
Q

How is HSV acquired?

A

Through close contact

  • from an infected person shedding virus
  • via skin contact or genital secretions
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32
Q

Describe HSV pathogenesis

A

HSV replicates initially in epithelial cells
- fluid filled blisters contain: detached epithelial cells, inflammatory cells, virions
The HSV penetrates dermis and enters sensory nerve axons
- enters latent stage, persistence for life

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33
Q

What are the steps involved in HSV pathogenesis?

A
  1. Initial entry to epithelial cells
    - lytic replication
  2. enters sensory neuron
    - travels to nucleus
  3. periodic reactivation
    - shedding back to epithelial cells
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34
Q

How many HSV infections are asymptomatic?

A

~70%

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35
Q

Describe primary lesions in HSV infection

A

They form 4-7 days after initial infection
Usually on penis, vulva (but may be intravaginal)
Symptoms: pain, itching, burning at site, dysuria
Overall symptoms: +/- fever, low grade headache, malaise, myalgias, inguinal lymphadenitis

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36
Q

How long do lesions from HSV take to heal?

A

3-4 weeks

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37
Q

How common are recurrent infections in HSV?

A

70-90% have recurrence within 1 year

Less severe than initial episode

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38
Q

Compare and contrast primary lesions and recurrent lesions

A 
Primary lesions
- multiple, widespread lesions at different stages
Recurrent lesions
- typically grouped
- identical stages of development
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39
Q

What are serious consequences of neonatal HSV?

A

Skin and eye disease
Cognitive impairment
Organ dysfunction
Death

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40
Q

How to prevent neonatal HSV from a mother with lesions?

A

Elective caesar

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41
Q

How do we diagnose HSV?

A

Initial diagnosis through clinical symptoms
Confirm by laboratory tests
- swab base of genital lesion, vesicle fluid
- send swab in viral culture medium

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42
Q

What are 3 methods of diagnosing HSV?

A

Viral culture
- poor sensitivity, HSV in <50% of recurrent lesions
PCR
- faster and ~4-times more sensitive than culture
HSV antigen detection
- Type specific IgG (HSV-1, -2) against glycoproteinG

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43
Q

What types of drugs are given for HSV infection and what do they do?

A

Antiviral drugs which reduce severity of symptoms and time to resolve
Give decreased viral shedding

44
Q

What are 3 drugs that can be given for HSV infection?

A

Acyclovir, Valacyclovir, Famciclovir

Orally or intravenously

45
Q

How do we prevent the transmission of HSV?

A
  • Abstain from sex if lesions present

- Use condoms consistently at other times

46
Q

Describe HPV

A

Double-stranded DNA virus
8kb genome
8 genes

47
Q

How many distinct types of HPV are there?

A

120
~40 types infect genital tract
~80% of females will acquire genital HPV infection by the age of 50

48
Q

What cancers is HPV linked to?

A 
Cervical
Anal
Vulvar
Penile
However, whilst HPV infection is necessary it is not sufficient
49
Q

Which HPV strains show strong links to cancer?

A

HPV-16 and -18 found in 64-79% of cervical cancers

HPV-31 and -45 also “high risk”

50
Q

How is HPV transmitted?

A

Via skin to skin contact

51
Q

Describe the pathogenesis of HPV

A

Enters squamous epithelium cells via microabrasions
- infection often resolved naturally
Viral proteins E6 and E7 disrupt cell division
- infected cells outgrow non-infected cells; resulting in warts and tumours
- may integrate into genome

52
Q

How is HPV diagnosed?

A

Clinical observation of lesions
Subclinical diagnosis: dilute acetic acid causes whitening of warts

Cytology

  • Papnicolaou (Pap) smear test
  • identification of cervical intraepithelial neoplasia (CIN) and early cervical cancers
53
Q

How do we treat HPV?

A

Cosmetic, non-specific, controls growth

- Liquid nitrogen, excision, causative agents

54
Q

How do we prevent HPV?

A

Preventative vaccine (Gardasil)

  • L1 virus structural protein
  • Virus like particles
  • nonavalent vaccine
55
Q

Which types of HPV are targeted by Gardasil?

A

6, 11, 16, 18, 31, 33, 45, 52, 58

56
Q

Effects of Chlamydia trachomatis

A

Chlamydia

~130 million infections/year

57
Q

Effects of Neisseria gonorrhoea

A

Gonorrhoea

~78 million infections/year

58
Q

Effects of Treponema pallidum

A

Syphilis

~6 million infections/year

59
Q

Effects of Haemophilus ducreyi

A

Chancroid

60
Q

What type of pathogen is Chlamydia trachomatis?

A

Obligate intracellular bacterial pathogen

ATP parasite

61
Q

What type of infection can C. trachomatis cause?

A

persistent, chronic infections

62
Q

What are the different serotypes of C. trachomatis and what type of disease do they cause?

A

A, B, C = serious eye disease trachoma
D-K = cause genital infection (chlamydia)
L1, L2, L3 cause the systemic STI lymphogranuloma venereum (infection in draining lymph nodes)

63
Q

How has the incidence of chlamydial infection changed since 2001.

A

Increased ~20% per year since 2001

64
Q

What are the steps in the C. trachomatis lifecycle?

A
  1. Attachment: Elementary body attaches to specific receptor on host cell
  2. Entry: parasite-specified endocytosis
  3. Differentiation to Reticulate body
  4. Multiplication of Reticulate body
  5. Differentiation of Elementary body
  6. Release: Elementary body progeny spread to adjacent cells
65
Q

Describe the Elementary body in C. trachomatis infection

A

Adapted for extracellular survival

Is metabolically inactive but stable extracellularly

66
Q

Describe the Reticulate body in C. trachomatis infection

A

Adapted for intracellular lifecycle

67
Q

Describe the symptoms of C. trachomatis infection

A

Symptoms observed 7-14 days after infection

Watery/mucopurulent discharge, dysuria

68
Q

What are some complications of C. trachomatis infection?

A 
Chlamydial cervicitis and urethritis
Both males and females may be asymptomatic
Female complications:
- Pelvic inflammatory disease
- Chronic pain
- Ectopic pregnancy
- Infertility
Complications rare in males
69
Q

How is C. trachomatis infection diagnosed?

A 
Its symptoms do not differentiate it from other STIs, therefore we must rely on the following:
Cell culture
- 100% specific, 48-72 hours
Direct antigen detection
- ELISA
- Direct immunofluorescence (low sensitivity)
PCR
- can use urine samples
- high sensitivity, fast 2-4 hours
70
Q

How is C. trachomatis infection treated?

A

Azythromycin - single dose

Tetracycline - doxycycline (10-day course)

71
Q

Are co-infections likely with C. trachomatis infection?

A

They occur in 5% of N. gonorrhoea infected patients

72
Q

Describe Neisseria gonorrhoea

A

Gram-negative bacteria
Only infects humans
Survives poorly in the environment

73
Q

What is N. gonorrhoea transmission called when transmitted vertically during vaginal delivery?

A

Ophthamia neonatorum

74
Q

Describe the pathogenesis of N. gonorrhoea

A
  1. Site of entry generally vagina or urethral mucosa of penis (also throat and rectal mucosa)
  2. Initial attachment facilitated by pili
    - high antigenic variation
    - outer membrane proteins (e.g. Opa) also important
  3. Invasion of non-ciliated epithelial cells
    - replication in vacuole
    - release through basement membrane
  4. Damage to host results from the host inflammaotry response
75
Q

What are the symptoms of N. gonorrhoea infection?

A

Symptoms observed within 2-7 days after initial infection
- vaginal or urethral (male) discharge
- Dysuria
Females often asymptomatic

76
Q

What are some complications of N. gonorrhoea?

A

Males = rare
Females:
- Pelvic inflammatory disease (10-20% of untreated cases)
- Chronic pelvic pain
- Fallopian tube damage and infertility
- Bloodstream infections (1-3% of cases) (septic arthritis)

77
Q

How is N. gonorrhoea infection diagnosed?

A 
Purulent discharge not reliably distinguishable from chlamydial discharge
Microscopy and culture:
- Smear of urethral discharge
- Gram-negative intracellular diplococci
- Organism very sensitive to drying
78
Q

How is N. gonorrhoea infection treated?

A

Ceftriaxone IM with azithromycin
Single treatment therapy
Ciprofloxacin or spectinomycin also useful

79
Q

Is N. gonorrhoea resistant to any antibiotics?

A

Yes, shows significant resistance to penicillins and increasing resistance to fluoroquinolones

80
Q

Is N. gonorrhoea infection notifiable?

A

Yes, must be notified to the Health Department and partner must be notified

81
Q

Does co-infection with N. gonorrhoea happen?

A

Yes, likely with chlamydia

82
Q

What pathogen causes Syphilis?

A

Treponema pallidum

83
Q

What are the 4 stages of T. pallidum infection?

A

Primary
Secondary
Latent
Tertiary: neurosyphilis, cardiovascular syphilis, congenital

84
Q

How is T. pallidum transmitted?

A

Sexual contact
- 15-30% risk of infection after sex with infected partner
Vertical transmission: mother to child in the placenta

85
Q

What is the incubation period of T. pallidum infection?

A

9-90 days

average is 2-4 weeks

86
Q

What is primary syphilis?

A

Lesions
Women: cervix, labia, urethra
Men: Penis, ano-rectal (MSM)
Lesions at extragenital sites uncommon (2-7%): fingers, lips, nipples

87
Q

What is secondary syphilis?

A 
Systemic spread of treponemes
7-10 weeks after primary lesion
- generally a skin rash
- highly infectious
Resolves in ~3 months
88
Q

What is tertiary syphilis?

A

In 3-30 years, 30% develop tertiary syphilis
Cell-mediated response
- Soft tissue destruction and gummas; granulomas resulting from chronic inflammation
- Cardiovascular; leaking of aortic valve
- Neurosyphilis; dementia and psychotic symptoms

89
Q

How is T. pallidum infection diagnosed?

A

Microscopy and serology
- No in vitro culture (culture in rabbits very slow)
Microscopy
- exudate from primary chancre (very infectious)
Non-treponemal tests
Treponemal tests

90
Q

How do non-treponemal tests diagnose T. pallidum?

A

Detect antibodies against cardiolipin (host membrane component-host damage) usually present in syphilis patients
RPR - Rapid Plasma Reagin test
VDRL - Venereal Disease Research Laboratory test
Low sensitivity (false negatives) and specificity (false positives)

91
Q

What does low sensitivity mean?

A

False negatives

92
Q

What does low specificity mean?

A

False positives

93
Q

How do Treponemal tests diagnose T. pallidum?

A

Enzyme immunoassay (ELISA for patient antibody)
TPHA - T. pallidum HaemAgglutination assay
FTA-ABS - Fluorescent Treponemal Antibody - Absorbed Test
High Specificity

94
Q

How is T. pallidum infection treated?

A

Historically:
- Heavy metals: mercury, arsenic compounds (Neosalvarsan)
- Malaria-induced fever (esp. for neurosyphilis)
Modern:
- Penicillin - high dose
-> doxycycline/Erythromycin if allergic

95
Q

How is T. pallidum infection prevented?

A

Safe sex

Secondary, tertiary and congenital syphilis prevention require early diagnosis and adequate treatment

96
Q

What pathogen causes Trichomoniasis?

A

T. vaginalis

97
Q

What is T. vaginalis?

A

Flagellated protozoan

98
Q

What are the symptoms of Trichomoniasis?

A 
Women:
- Cervicitis
- Malodorous profuse frothy vaginal discharge
- Itchy/soreness
~50% women are asymptomatic
Most men are asymptomatic
- unusually dysuria and penile discharge
99
Q

What is the route of transmission of T. vaginalis?

A

Vaginal, oral or anal sexual intercourse

100
Q

How is T. vaginalis infection diagnosed?

A

PCR on first pass urine or high vaginal swab

101
Q

How is T. vaginalis infection treated?

A

Metronidazole (flagyl)
- 2g orally once or 400mg for 5 days
or Tinidazole

102
Q

What is Candida albicans?

A

Diploid fungus

Normal oral, gut and vaginal flora

103
Q

What infection does Candida albicans cause?

A

overgrowth -> vaginal candidiasis (thrush)

104
Q

What are the symptoms of C. albicans infection?

A

Irritation
Inflammation
Cheesy discharge
+/- dysuria

105
Q

What are predisposing factors of C. albicans infection?

A

Hormone changes (menses, pregnancy)
Diabetes
Reduced cell-mediated immunity
Antibiotic treatment

106
Q

In who is C. albicans most likely to cause systemic infection?

A 
AIDS patients
Transplant patients
Cancer patients
Burns patients
Anyone with an immunodeficiency
107
Q

How is C. albicans infection treated?

A

Topical or oral antifungal

MIC3041 Medical Microbiology (11 decks)

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