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MIIM20002 - Microbes, Infections, Responses > Lecture 26 - Sexually Transmissable Infections 1 > Flashcards

Lecture 26 - Sexually Transmissable Infections 1 Flashcards

1
Q

Which general organisms can cause STIs?

A
  • Bacteria
  • Viruses
  • Protozoans
  • Fungi
  • Arthropods (lice)
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2
Q

Which bacteria cause STIs?

A
  • Chlamydia trachomatis
  • Neisseria gonorrhoeae
  • Treponema pallidum
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3
Q

Where do STIs cause infection?

A 
Female: all areas of genital tract
• vaginitis
• cervicitis
• endometritis
• salpingitis
• urethritis
Male: 
• urethritis
• epididymitis
• proctisis
• prostatitis
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4
Q

What is the name for inflammation of the Fallopian tubes?

A

Salpingitis

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5
Q

Why is dealing with STIs difficult?

A
  • Stigma
  • Embarrassment
  • Morals
  • Tendency to ignore the infection

→ even though we have good treatment and prevention, we can’t eradicate them

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6
Q

What can salpingitis lead to?

A

Infertility

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7
Q

What are the common features of STIs?

A
  • Shared mode of transmission
  • Shared mode of prevention

• All may be asymptomatic

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8
Q

How is HIV transmitted

A

• Sexual route
Also, other routes:
• needles
• congenital

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9
Q

What does ‘STIs hunt in packs’ mean?

A

More than one infectious rate present at once

One infection facilitates the uptake of other agents as well

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10
Q

Under what conditions is HIV transmission rate increased?

A

Underlying STI → altered barriers

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11
Q

Can an infection be transmitted from asymptomatic individuals?

A

Yes

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12
Q

What is the main cause of damage in STIs?

A

Immune response

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13
Q

What are the animal reservoirs of the bacteria causing STIs?

A

No animal reservoir

Human pathogens only

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14
Q

In general, how are STIs treated?

A

Antibiotics

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15
Q

In general, how are STIs prevented?

A

Condoms

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16
Q

Which is one of the most common STI in young people in Australia?

A

Chlamydia

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17
Q

What infections do Chlamidia trachomatis serovars A,B and C cause?

A

Trachoma

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18
Q

What is trachoma?

How is it caused?

A

Ocular infection, scarring of eye and eyelids

Repeated infection with Chlamydia

Especially seen in Aboriginal populations in Australia

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19
Q

How can trachoma transmission be stemmed?

A

Eye washing

Because flies move the eye secretions between individuals

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20
Q

What do serovars D-K cause?

A
  • Conjunctivitis
  • Urogenital tract infections
  • Reactive arthritis
  • Pneumonitis
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21
Q

What do serovars L1-L3 cause?

Where are these infections commonly seen?

A

• Lymphogranuloma venereum

  • Invades lymph nodes of genital tract
  • Abscesses form
  • Africa, India, South America
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22
Q

What does Chlamydophila pneumoniae cause?

A

Atypical pneumonia

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23
Q

What does Chlamydophila psittaci cause?

What is this infection associated with?

A

Acute respiratory disease

Associated with birds

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24
Q

How many cases per year of C. trachomatis in Victoria?

Why so many?

A

10,000

People don’t know they have it

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25
Q

Which sites are commonly infected with serovars D-K?

A 
Cervix
Urethra
Pharynx
Rectum
(Conjunctivitis)

May also be:

  • endometritis
  • salpingitis
  • epididymitis
  • proctitis
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26
Q

What does serovar D-K infection present as?

A

Discharge in males and females

Watery (non-puralent)

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27
Q

Can chlamydia be spread congenitally?

A

Yes, during vaginal delivery, bacteria may get into eye or be inhaled

Conjunctivitis
Pneumonia

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28
Q

Describe the morphology of Chlamydiae spp.

A

Gram negative
V. small

No peptidoglycan

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29
Q

Why can Chlamydiae spp. be gram stained?

A

No peptidoglycan → can’t be gram stained

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30
Q

Describe the LPS in Chlamidae spp.

A

Truncated

Not very endotoxic

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31
Q

Describe the replication of Chlamydia spp.

A

Obligate intracellular replication
because it is an energy parasite (required ATP)

2 stages:
• Elementary body (EB)
• Reticulate body (RB)

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32
Q

How do we culture Chlamydia?

A

Must be cultured in cells

Because it is an energy parasite

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33
Q

What are the EB and RB ?

A

EB: non-replicating
• infectious
• extracellular

RB: actively replicating
• intracellular
• non-infectious

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34
Q

Which cells does Chlamidae spp. infect?

A

Columnar epithelial cells

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35
Q

Describe Chlamydia entry into cells

A
  1. EB bind with adhesins
  2. Receptor mediated endocytosis
  3. Lysosome doesn’t fuse
  4. Inclusion forms
  5. EB → RB
  6. RBs replicate inside inclusions
  7. RB → EB
  8. EB released in secretions
  9. Spread to other people
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36
Q

What is an inclusion?

A

Fusion of endosomes containing chlamydia bacteria

Contain 200-1000 bacteria

37
Q

How do bacteria in an inclusion get nutrients?

A

‘Drinking straws’ inserted into host cytoplasm

38
Q

Which form of chlamydia is susceptible to anti-microbial agents?

A

Reticulate bodies only

39
Q

What is the effect of IFN-gamma on chlamydia?

Where is this coming from?

A
  • Prolonged RB phase
  • Persistance
  • Low grade chronic inflammation

IFN-gamma is coming from activated T cells

40
Q

Describe the immune response to chlamydia

A
  1. Infected epithelial cells produce chemokines and other inflammatory mediators
  2. Influx of neutrophils, monocytes, DC, NK
  3. T and B cell activation
  4. Lymphocytes and macrophages form follicles
  5. Chronic inflammation
  6. Scar tissue formation
41
Q

What toxin that chlamydia produces can cause damage?

A

hsp60
Heat shock protein

Persistent inflammation

42
Q

How do we diagnose chlamydia infection?

A
  1. Collect sample
    2a. PCR
    2b. EIA, immunofluorescence
43
Q

What samples are collected for diagnosing chlamydia?

A

Cervical and urethral swabs

First pass urine

44
Q

How is chlamydia infection treated?

Why these ones?

A

Tetracycline
Macrolide antibiotics
Azithromycin

They are good at penetrating into the cells

45
Q

Describe the morphology of Neisseria gonorrhoeae

A

Gram negative

Diplococcus

46
Q

Is Neisseria gonorrgoeaea hardy?

A

Not at all

Susceptible to drying
Susceptible to disinfectants
Extremely fastidious

47
Q

In what conditions do N. gonorrhoeae grow best?

A

CO2 enriched

48
Q

What are the clinical presentations of gonorrhoea?

A

Similar to chlamydia

49
Q

Are symptoms always seen in gonorrhoea?

A

Females: Asymptomatic infection is common

Males: less so

50
Q

To where does N. gonorrhoea somtimes spread in females?

A

Ascending genital tract:
Pelvic inflammatory disease

Disseminate throughout the body

51
Q

Under what circumstances will babies get gonorrhoea?

Describe the infection in babies

A

Congenital transmission from their mothers

Extremely purulent conjunctivitis

52
Q

Which groups are most commonly infected with gonorrhoea in Australia?

A

Men who have sex with men
Infection from overseas
- SE Asia sex tour

Aboriginal communities

53
Q

What is important about gonorrhoea infections from overseas?

A

More profound antibiotic resistance

54
Q

Which cells are infected by N. gonorrhoeae?

A

Columnar epithelial cells

55
Q

Describe the gonorrhoea pathogenesis

A
  1. Adhesins binds
  2. Replicate on cell surface
  3. Spread in mucosal secretions

(May occasionally infect cells and disseminate)

56
Q

What are the gonorrhoeal adhesins?

A

Pili
Outer membrane proteins
Lipo-oligosaccharide

57
Q

Describe dissemination of gonorrhoea

A

Strain specific
ie not all strains will do this normally

Dissemination occurs when there is poor complement and neutrophil activation (to keep it at the site)

58
Q

How does gonorrhoea cause damage?

A

Inflammatory response

No exotoxins

59
Q

Outline the inflammatory response to gonorrhoea

A
  1. LPS and peptidoglycan interat w/ PRR
  2. Pus, pain
  3. TNF production → loss of ciliated epithelial cells
  4. Avoidance of C’ cascade and neutrophils
60
Q

Which damage is more severe, that of chlamydia or gonorrhoea?

A

Gonorrhoea

61
Q

What does TNF production during gonorrhoea infection bring about?

A

Loss of ciliated epithelia

62
Q

Why is there poor complement and neutrophil activation in gonorrhoea infection?

A

Because the altered LPS doesn’t stimulate this as well

63
Q

How does gonorrhoea avoid antibody responses?

A

Antigenic variation
of the pili and surface proteins at high frequency

Escape the antibody response

64
Q

Describe horizontal transmission of genetic material in gonorrhoea bacteria

A

Readily take up DNA from other sources

  • plasmids
  • transposons

Implications:
- rapid antibiotic resistance

65
Q

How do we diagose gonorrhoeal infection?

A
  1. Swab collection, discharge collection
  2. Gram stain + microscopy
    Males: presence of diplococci (intracellular and extra. is diagnostic

PCR

66
Q

Which samples must be collected in order to perform PCR?

A

Urine

Vaginal swab

67
Q

How do we culture N. Gonorrhoeae?

A

GC: gonoccocus medium
or Chocolate agar

Fastidious
Need to select out normal flora in sample

Won’t grow on HBA

68
Q

Describe the bi-plate

A

Both sides: lysed HBA (GC)

One side: antibiotic
- only gonococci will gorw
Other side: no antibiotics

This allows us to find the gonococci amongst the normal flora

69
Q

Describe treatment of gonorrhoea

A

Check guidelines for ‘Empiral’ treatment

Beta-lactamase resistance cephalosporin
- Ceftriaxone

Azithromycin

70
Q

What does Treponema pallidum cause?

A

Syphilus

71
Q

Describe morphology and staining of T. pallidum

A

Spirochete: spiral rod

Can’t be Gram stained
- need special Dark-ground microscopy

72
Q

Describe the motility of T. pallidum

A

Corkscrew like movement

Periplasmic contractile flagella

73
Q

Is T. pallidum hardy?

A

Not at all

Very labile

74
Q

How do we culture T. pallidum?

A

non-culturable

75
Q

Is syphilis common in Australia?

A

Rates dropped amongst homosexuals

Epidemics in heterosexuals recently
- fly-in fly-out mining communities

76
Q

Can babies get syphilis?

A

Bacteria cross the placenta in utero

77
Q

Are there always symptoms with syphilis?

A

Not always

Asymptomatic as well as symptomatic

78
Q

In general, describe the stages of syphilis

A
  1. Infection
  2. Primary syphilis
  3. Secondary syphilis
  4. Tertiary syphilis
79
Q

What is primary syphilis?

How long does it last?

A

• Local ulcer
• Chancre
(on penis)

Can be asymptomatic

• 2-6 weeks

80
Q

What is secondary syphilis?
When does it occur?

How long does it last?

A
  • Rash
  • Warty genital lesions
  • Lymphadenopathy

Occurs if the 1° infection isn’t treated, or if asymptomatic

• Lasts up to 6 months

81
Q

How long the asymptomatic period between 2° and 3° syphilis last?

A

3-30 years

82
Q

When will syphilis infection be transmitted from person to person?

A
  • Local ulcer

* Disseminated bacteria

83
Q

What is tertiary syphilis?

A
  • Gummas
  • Eyes
  • Ears
  • Heart
  • Brain
84
Q

How is syphilis diagnosed?

A
  1. Droplet from lesion
  2. Dark-ground microscopy
  3. PCR
  4. Serology
85
Q

What does serology tell us about T. pallidum?

A

Detection of antibodies to treponemal antigens

Cross reactive antibodies

86
Q

Describe the features of the Rapid plasma reagin test

A

Measures antibodies made against cariolipin

Highly sensitive (few false negatives)
Not very specific (some false-positives)
Cheap
87
Q

How is syphilis treated?

A

Penicillin

88
Q

When are gummas seen?

What are they?

A

Tertiary Syphilis

They are a type of granuloma

89
Q

What is controlling syphilis in the asymptomatic period?

A
  • Macrophages
  • Th cells
  • B cells

MIIM20002 - Microbes, Infections, Responses (32 decks)

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