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Micro 3010 > Unit 14 - STI's > Flashcards

Unit 14 - STI's Flashcards

1
Q

List the STI’s that will be covered in this lecture

A
  • syphilis
  • gonorrhea
  • chlamydial infection
  • genital herpes
  • HPV
  • HIV
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2
Q

What is syphilis caused by?

A

Treponema pallidum

subspecies = pallidum

*invasive organism

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3
Q

How many new cases/yr worldwide of syphilis?

A

11 million

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4
Q

Syphilis is more common in which gender?

A

male

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5
Q

Syphilis:

Incubation time?

A

1-90 days

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6
Q

Syphilis:

3 phases

A

1) Primary
2) Secondary
3) Tertiary (late)

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7
Q

Syphilis:

Describe the primary phase

A
  • Chancres (skin lesions) at site of inoculation
  • Usually painless & heal spontaneously
  • Highly infectious
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8
Q

Syphilis:

Describe the secondary phase

A
  • signs of disseminated (widely spread disease)
  • 2-12 weeks after infection
  • skin lesions on truck, palms, & soles of feet
  • LESION FLUID HIGHLY INFECTIOUS
  • signs of other organ involvement
  • 3-12 weeks, disappearance of symptoms
  • latent phase follows
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9
Q

Syphilis:

Describe the latent phase

A

-asymptomatic
-antibodies present
-three outcomes (untreated patients)
1-relapse
2-no relapse
3-tertiary phase

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10
Q

Syphilis:

Describe the tertiary phase

A
  • can occur long after initial infection
  • neurologic cardiovascular symptoms
  • may have gummas (nonspecific granulomatous lesions)
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11
Q

What is congenital syphilis?

A
  • Mothers with untreated/improperly treated syphilis
  • Signs of secondary syphilis at birth
  • Prevented if women are screened in early pregnancy and treated with penicillin
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12
Q

Syphilis:

What is used for lab diagnosis?

A

Dark field of fluorescent microscopy

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13
Q

Syphilis:

List 3 types of serodiagnosis

A

1 - Nontreponemal antibodies

2 - Treponemal antibodies

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14
Q

Syphilis:

Describe serodiagnosis performed with nontreponemal antibodies

A

VDRL: general disease release laboratory test

RPR: rapid plasma reagin test

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15
Q

Syphilis:

Describe serodiagnosis performed with treponema antibodies

A

FTA-ABS: fluorescent treponema antibody absorption

Agglutination tests

  • MHA-TP (microhemagglutination test)
  • TP-PA test (treponema pallidum particle agglutination test)
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16
Q

Syphilis:

Treatment

A

penicillin, doxycycline

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17
Q

Syphilis:

Prevention of secondary and tertiary syphilis

A

early diagnosis and treatment

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18
Q

Gonorrhoea:

What is the cause?

A

Neisseria gonorrhoeae

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19
Q

Gonorrhoea:

Describe Neisseria gonorrhoeae

A

gram negative diplococci

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20
Q

Gonorrhoea:

Where does Neisseria gonorrhoea affect the human body?

A
  • cervix, uterus, and fallopian tubes (female reproductive tract)
  • urethra (males &females)
  • mouth, throat, eyes, anus
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21
Q

Gonorrhoea:

Women have a ____% chance of infection post single encounter

A

50%

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22
Q

Gonorrhoea:

Men have a ____% chance of infection post single encounter

A

20%

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23
Q

Gonorrhoea:

Vertical transmission results in _____ ________

A

opthalmia neonatorum

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24
Q

Neisseria gonorrhoeae are ______

A

capnophiles

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25
Q

What are capnophiles?

A

capnophiles are microorganisms that thrive in the presence of high concentrations of carbon dioxide

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26
Q

Neisseria gonorrhoeae likes ____ atmospheres

A

humid

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27
Q

______ new cases of gonorrhoea/yr worldwide

A

97 million

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28
Q

Gonorrhoea:

List the virulence factors

A 
pilus
por proteins
opa proteins
LOS
Rmp proteins
IgA protease
capsule
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29
Q

pilus

A

aid attachment to human mucosal epithelium; contains constant and hyper variable regions - analogous to immunoglobulins (Igs) - that contribute to antigenic diversity in gonococci

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30
Q

por proteins

A

form pores through outer membrane; antigenic; specific serotypes associated with virulence

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31
Q

opa proteins

A

assit binding to epithelial cells

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32
Q

LOS

A

lipooligosaccharide (endotoxin activity)

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33
Q

Rmp proteins

A

inhibit ‘cidal’ activity of serum

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34
Q

IgA protease

A

core contains enzyme; released by cell to destroy IgA 1

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35
Q

capsule

A

resists phagocytosis, unless antibody present

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36
Q

Gonorrhoea in females is often ________

A

asymptomatic

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37
Q

If gonorrhoea is present in females, it will develop in ____ days

A

2-7

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38
Q

Symptom of gonorrhoea in females?

A

vaginal discharge

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39
Q

Untreated complications of gonorrhoea in females?

A
  • PID
  • chronic pelvic pain
  • infertility
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40
Q

Symptoms of gonorrhoea in males?

A
  • urethral discharge

- painful urination

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41
Q

Other conditions of gonorrhoea?

A
  • Anorectal (purulent discharge), pharyngeal (sore throat) & ophthalmic infections
  • Ophthalmia neonatorum in newborns
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42
Q

Diagnosis of gonorrhoea uses a _____ ______

A

gram stain

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43
Q

Urethral discharge from symptomatic males with urethritis is caused by??

A

gram negative diplococci inside PMN’s

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44
Q

Gonorrhoea:

gram stain is not as useful for women - why?

A

normal vaginal and rectal flora have G-coccobacilli

45
Q

Gonorrhoea:

gram stain is not as useful for women - how do you diagnose instead?

A

must confirm diagnosis by culture

46
Q

Gonorrhoea:

Treatment?

A

antibiotics

*key concern is resistance

47
Q

Is there immunity for gonorrhoea?

48
Q

What makes up the largest proportion of STIs reported in Canada and the US ?

A

genital chlamydiosis

49
Q

Genital chlamydiosis:

______ new cases in 1999, worldwide

A

92 million

50
Q

Genital chlamydiosis:

What causes it?

A

obligate intracellular bacterium

51
Q

Genital chlamydiosis:

Serotypes L1, L2, and L3 cause?

A

1) STIs
- lymphogranuloma venerum (LGV)
- genital chlamydiosis
- nongonococcal urethritis

2) ocular and respiratory infections

52
Q

Genital chlamydiosis:

Serotypes A-C cause?

A

trachoma (bacterial infection of the eye)

53
Q

Genital chlamydiosis:

Describe the life cycle of chlamydia

A
  • Elementary body binds host columnar epithelial cells
  • Enters epithelial cell -> forms reticulate/initial body -> replicates by binary fission -> inclusions -> elementary bodies -> release form cell -> infectious cycle

*see slide 21 for life cycle

54
Q

Genital chlamydiosis:

Describe the diagram from slide 21 (the life cycle of chlamydia)

A
  • attachment (EB attaches to specific receptor on host cell)
  • entry (parasite-specified endocytosis)
  • differentiation to RB
  • multiplication of RBs
  • differential to EBs
  • release (EB progeny spread to adjacent cells)
  • EB = elementary body
  • RB = reticulate body
  • from entry to differentiation to RB = takes 9-10 hours
  • from differentiation to Rb to release = 20 hours
55
Q

Genital chlamydiosis:

Describe the presumptive diagnosis of chlamydia

A
  • clinical suspicion based on symptoms

- positive non culture result (EIA, DFA, or nucleic acid detection)

56
Q

Genital chlamydiosis:

Describe the definitive diagnosis of chlamydia

A

-culture and ID of inclusion bodies
OR
-combination of 2 non culture methods

57
Q

List 2 other possible causes of vaginitis and urethritis

A

1) Candidiasis

2) Trichomoniasis

58
Q

What is candidiasis caused by?

A

C. albicans

*causes 80-90% of vaginal candidiasis

59
Q

Carriage

A

Is when a bacteria jumps onto an object or individual, but is then quickly removed – so it is there only for a brief period of time.

60
Q

Infection

A

Is the invasion of an organism’s body tissues by disease-causing agents, their multiplication, and the reaction of host tissues to these organisms and the toxins they produce.

61
Q

Symptoms of vaginitis and urethritis caused by Candidiasis

A

itching, erythema, discharge: nil to thick

62
Q

Treatment of vaginitis and urethritis caused by Candidiasis

A

OTC drugs - possible resistance?

63
Q

What causes Trichomoniasis?

A

Trichomonas vaginalis

64
Q

Trichomonas vaginalis is a ______ parasite

65
Q

Trichomoniasis produces what kind of discharge?

A

profuse, offensive, yellow-green

**can be asymptomatic

66
Q

Treatment for trichomoniasis?

A

Metronidazole

67
Q

Genital herpes is caused by what virus?

68
Q

HSV-1 transmitted by ____

69
Q

What does HSV-1 cause?

A

Oropharyngeal infections in children, cold-sores after reactivation

70
Q

How is HSV-2 spread?

A

venereal route

71
Q

What is genital herpes characterized by ____ _____

A

ulcerating vesicles

72
Q

Primary lesions appear on penis/vulva ____ days post infection

73
Q

Genital herpes:

Break down to form painful ulcers which lead to ??

A

swollen lymph nodes, fever, headache, malaise

74
Q

Genital herpes:

Healings takes how long?

75
Q

Genital herpes:

Describe the pathophysiology

A

virus, lesion -> sensory nerve ending -> latent infection in dorsal root ganglion neurons

76
Q

Genital herpes:

Describe reactivation

A

reactivation, travel down same route -> recurrent lesions (genital cold sores)

77
Q

Genital herpes:

Mother to infant during birth -> ??

A

neonatal disseminate herpes or encephalitis

78
Q

Genital herpes:

Diagnosis ?

A
  • Virus DNA in vesicle fluid or ulcer swabs

- Immunofluorescence

79
Q

Genital herpes:

Treatment?

A

Antivirals

80
Q

Genital herpes:

Recurrent infections can be troublesome - how do we combat this?

A

6-12 months of low dose antiviral to stop/reduce frequency of recurrences

81
Q

HPV

A

human papilloma virus

82
Q

HPV causes

A
  • papillomas/warts

- cervical cancer

83
Q

There are ___ distinct types of HPV

84
Q

____ genital types of HPV

85
Q

Can HPV be grown in culture?

86
Q

How can you diagnose HPV?

A

Cytology sections

  • Pap smears
    • Koilocytes

Nucleic acid detection
-PCR

87
Q

HPV:

Vaccine available?

A

Yes

Quadrivalent vaccine

88
Q

HPV:

What types are in the quadrivalent vaccine?

A

HPV types 6, 11, 16, and 18

89
Q

HIV

A

human immunodeficiency virus

90
Q

HIV is a ______

A

retrovirus (lentivirus) - slow virus

91
Q

What is a retrovirus?

A

A retrovirus is a single-stranded positive-sense RNA virus with a DNA intermediate and, as an obligate parasite, targets a host cell.

92
Q

What is a lentivirus?

A

is genus of retroviruses that cause chronic and deadly diseases characterized by long incubation periods, in man and other mammalian species.

*basically a slow retrovirus

93
Q

HIV is isolated from??

A

blood lymphocytes

94
Q

HIV likely started in ____

95
Q

HIV-1 and HIV-2 arose from closely-related _____ viruses

96
Q

List the 3 groups of HIV-1

A

M (Main)
N (New)
O (Outlier)

97
Q

Describe M (Main) type of HIV-1

A

A-J

  • B most common in NA and Europe
  • A & C
98
Q

Describe N (New) and O (Outlier) type of HIV-1

A

West Central Africa

99
Q

Increased _____ is causing a change in subtype distribution

100
Q

HIV infects cells with ____ surface marker

A

CD4

ex. Th cells

101
Q

HIV:

Describe the Pathogenesis

A

1) Entry: binding of viral gp120 envelope glycoprotein to CD4 receptor

2) chemokine co-receptor (CCR5) - establishing infection
* individuals with CCR5 gene deletions are resistant
* disease progression seen with HIV variants using CSCR4 receptor

3) Viral replication halts after integration of provirus (latent in cell)
* see slide 32 for diagram

102
Q

Routes of transmission:

___% infants infected in utero and intrapartum

103
Q

Routes of transmission:

____% post-natally

A

11-16%

*associated with breastfeeding for up to 24 months

104
Q

Clinical definition of HIV

A

CD4+ count, 200 mm^3 (> 1000 mm^3)

105
Q

HIV:

Describe Treatment

A

HAART (highly active antiretroviral therapy)

106
Q

HIV:

Describe Drawbacks

A
  • Mitochondrial toxicity and altered fat distribution
  • HIV inhabits CSF and GU tract
    • Drugs cannot reach, high load in semen
  • Resistance
107
Q

HIV:

Diagnosis

A
  • Serological (HIV-1 & HIV-2 Abs)
  • Molecular analysis - detect HIV-1 RNA or proviral DNA
  • Measuring load of HIV-1 RNA also performed (RT-PCR)
108
Q

Which STI’s have vaccines?

A

hepatitis and HPV

109
Q

____ intervals between the onset of infectiousness and disease increase the chances of transmission

Micro 3010 (20 decks)

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