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Second Year Microbiology > STIs > Flashcards

STIs Flashcards

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1
Q

What are common features of STIs?

A

• Shared mode of transmission (sexual)

  • =shared mode of prevention
  • More than one infectious agent often present (hunt in packs)
  • Enhances HIV transmission/acquisition
  • Can be asymptomatic and transmissible
  • Often persistent infections with significant consequences
  • Stigma can prevent treatment, possible eradication
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2
Q

What are the features and examples of bacterial STIs?

A
  • Chlamydia tranchomatis
  • Neisseria gonorrhoea
  • Treponema pallidum
  • Very infectious, easy spread
  • Humans only
  • Effective antibiotic treatment
  • Prevent with condoms
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3
Q

What are part of the Chlamydia genus? Where do they cause infection?

A

Chlamydia tranchomatis

  • Serovars A,B,C – trachoma
  • Serovars D-K – conjunctivitis, urogenital tract infections, pneumonitis
  • Serovars L1-L3 – lymphogranuloma venereum

Chlamydophila pneumonia – atypical pneumonia

Chlamydophila psittaci – acute respiratory disease

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4
Q

What are features of Chlamydia trachomatis serovars D-K?

A
  • Most common bacterial STI (developed world)
  • Many asymptomatic
  • Can infect eye • Discharge
  • Can ascend upper genital tract cause infection and damage
  • Can be passed to newborns
  • Persistent infections common
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5
Q

What are features of Chlamydiae bacteria?

A
  • Gram negative
  • Small
  • Wont detect peptidoglycan in cell wall (no gram stain)
  • Observe lymphocyte response
  • LPS truncated, not very endo-toxic
  • Obligate, intracellular (need host mitochondria for energy)
  • Therefore need cell culture
  • Slow replication with EB and RB stage
  • Damage due to host immune response
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6
Q

What’s involved in the replication cycle of Chlymadiea?

A

• Slow and 2 development stages (elementary body/EB and reticulate body/RB)

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7
Q

What happens during chlamydia entry, multiplication and spread?

A
    1. Elementary body (binds columnar epithelial cells by adhesins, RME
    1. Endosome with EB doesn’t fuse with lysosome (no destruction). Endosomes fuse to form inclusions
    1. EB transformed to metabolically active reticulate body. RB replicates in inclusions
    1. RB converted to EB and EB released
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8
Q

What are EB and RB and how do they differ?

A
  • elementary body = infectious, extracellular particle (no replication, no antimicrobial susceptibility)
  • reticulate body = intracellular, replicative, don’t survive outside cells, targeted by microbials but they need to penetrate cell and tissue, If IFNγ present (from T cells, macrophage), prolong RB phase, low grade chronic inflammation and tissue damage
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9
Q

How does chlamydia cause damage?

A
  • Infected epithelial cells, make chemokines so influx of neutrophils, monocytes, DCs, NK cells
  • T and B cells activated and accumulate to form follicles
  • Continuing activation = chronic inflammation
  • Persistent inflammation due to hsp60 from chlamydial
  • Recurrent infections
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10
Q

How can chlamydia be diagnosed and treated?

A
  • Swabs, first pass urine specimens
  • PCR
  • EIA less common
  • Tetracycline or macrolide antibiotics
  • Good penetration
  • Given over prolonged time

• azithromycin

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11
Q

What is the preferred treatment for chlamydia?

A

• Single dose long acting macrolide/azithromycin ideal

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12
Q

What are the features of Neisseria gonorrhoea?

A
  • Gonorrhoea
  • Gram negative diplococcus
  • Intracellular mostly
  • Likes to grow in Co2 (but not anaerobe)
  • Similar clinical presentation to chlamydia
  • Symptomatic = urethritis
  • Can ascend in females, cause pelvic inflammatory disease (PID)
  • Predominately for gays
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13
Q

How does gonorrhoea enter, spread and multiply in us?

A
  • Target columnar epithelial cells like chlamydia
  • Attach with adhesins (pili, OM proteins, LPS with no O antigen/lipo-oligosaccharide)
  • Cell surface replication • Spread in mucus secretions (pili twitching motility)
  • And invade and go to sub-epithelial tissue, Inflammation/dissemination
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14
Q

Why is complement and neutrophil activation poor by gonorrhoea?

A

• Poor complement/neutrophil activation because altered LPS and lack some OM proteins

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15
Q

How does gonorrhoea cause damage?

A
  • No exotoxins
  • Inflammatory response (PRR, LPS, peptidoglycan)
  • Pus, pain
  • TNF causes loss of ciliated epithelial cells
  • Invasive strains avoid complement cascade/neutrophils
  • Prolonged infection due to antigenic variation in pili, surface proteins
  • Can acquire other genetic material (antibiotic resistance)
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16
Q

How is gonorrhoea diagnosed?

A
  • Culture and gram stain
  • PCR
  • Microscopy (gram neg diplococcic and polymorphonuclear neutrophils)
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17
Q

What kind of culture is needed for gonorrhoea and why?

A
  • Often normal flora present, need selective enriched medium
  • Gonococcus Medium (GN)
  • Lysed HBA biplate
  • One side antibiotics, selective for Gonococcus
  • Culture essential for working out antibiotic susceptibility
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18
Q

How can gonorrhoea be treated?

A
  • Check guidelines
  • Beta-lactamase resistant cephalosporin
  • Also use azithromycin as 40% have chlamydia too
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19
Q

What causes syphilis? What are the features of this bacterium?

A
  • Treponema pallidum
  • Spirochaete family (some normal microflora)
  • Slender, spiral rod, need special to visualise
  • Motile with contractile flagella
  • Labile, easy to inactivate
  • Non culturable
  • Possible spread from placenta to foetus
  • Asymptomatic or symptomatic
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20
Q

What are the stages of syphilis infection and what is involved in each stage?

A

Infection

  • 3 weeks
  • Multiply and disseminate into blood/tissue

Primary syphilis

  • Local ulcer (chancre)
  • Or asymptomatic (2-24 weeks)
  • 2-6 weeks – control by immune system, resolution or continuation

Secondary syphilis

  • Genital lesions, rashes, warts
  • Bacteria localise in tissue to cause symptoms
  • Asymptomatic (3-30 years)
  • 2-6 weeks – control by immune system, resolution or continuation

Tertiary syphilis

  • Targets other important organs
  • Multiplication and hypersensitivity response
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21
Q

How long can someone be asymptomatic at each stage of syphilis infection?

A
  • Primary 2-24 weeks
  • Secondary 3-30 years
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22
Q

How is syphilis diagnosed?

A

Dark ground microscopy and PCR rarer

Serology

  • Detect antibodies to treponemal antigens
  • Rapid plasma reagin test (RPR)
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23
Q

What is the basis of the rapid plasma reagin test?

A
  • Measure abs made against components of damaged cells – cardiolipin
  • Very sensitive (not many false negatives)
  • Not very specific (some false positives)
  • Cheap
  • Screening test
  • Need confirmation with specific tests, EIA
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24
Q

How is syphilis treated?

A
  • Sensitive to penicillin
  • No resistance
  • Need to prevent progression
  • Need to prevent congenital syphilis (screen pregnant mums)
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25
Q

What is an important feature of viral STIs?

A

• They are persistent

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26
Q

What are features of the herpesviridae family?

A
  • Large
  • Icosahedral
  • Enveloped
  • Ds DNA, Linear
  • Encode array of proteins
  • Can be latent in host
  • Very common
  • Also VZC, glandular fever, roseola
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27
Q

What is the structure of HSV?

A
  • Glycoproteins on outside
  • Envelope

o Means virus is labile

o Requires intimate contact

o Transmitted in bodily fluids

• Tegument proteins

o Unique to herpes

o Infection and evasion

• Icosahedral capsid

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28
Q

What are the features of HSV? How can you distinguish HSV 1 and 2?

A
  • Serotypes HSV1 and HSV2
  • Distinguish with serological testing (antigen detection) and PCR (gene detection)
  • Both cause localised infections and disseminated infections
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29
Q

What disseminated infections can result from HSV?

A

• meningoencephalitis, encephalitis

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30
Q

How can HSV stay latent?

A
  • Go from epithelial cells to dorsal root ganglia (infect sensory neurons then transported)
  • HSV maintained as episome and doesn’t replicate (linear DNA now closed circular)

o = latency

o Genome circularises (episome) in neural cells

o Few viral genes expressed

o Produces latency activated transcript RNAs (but no resultant protein)

o HSV 1 infected ganglia often associated with T cells, cytokine and chemokine’s, suggest immune stimulation

• Reactivation from ganglia = recurrent infections at original site

o Certain stimuli (UV, stress, fever) reactivates from episomal state

o Goes down sensory nerve

o Reactivation at original site

• Rarely, can go from ganglia to CNS instead

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31
Q

How does HSV enter a cell? Why is direct contact required?

A
  • Target cells: epithelial, fibroblasts, macrophage
  • Infects skin and mucous membranes
  • Direct contact (labile enveloped virus)
  • Glycoproteins on envelope

o gpB and gpC

o Bind cell surface receptors (heparan sulphate)

o Binding on it’s own not enough for entry

o Bind triggers fusion of envelope with cell membrane, nucleocapsid released to cytoplasm

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32
Q

How does HSV replicate in epithelial cells?

A
  1. Binding, membrane fusion
  2. Capsid released to cytoplasm, then translocated to nucleus
  3. Early genes and mRNAs
  4. Early proteins (non-structural)
  • DNA polymerase(replication)
  • Thymidine kinase
  • ICP47 (Inhibits MHC I presentation and expression)
  1. DNA synthesis
  2. Late genes and structural proteins
  3. Assembly
  4. Release
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33
Q

How can HSV affect epithelial cells?

A
  • Replication means lots of infectious virus released
  • Causes cell death
  • Cell to cell spread/infection
  • Loss of epithelial cells = lesions/ulcer
  • Infection can be asymptomatic
  • Transmission whilst symptomatic or asymptomatic
  • Can spread to CNS (meningitis etc.) – rare
  • Move on to become latent
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34
Q

What are the features of HSV 1 and 2? How are they different?

A

HSV 1

  • Spread by saliva
  • Cold sores,
  • encephalitis
  • 70-80% antibody positive
  • 1% asymptomatically secrete

HSV 2

  • Spread by genital secretions
  • Genital herpes, neonatal herpes
  • 12.5-25% antibody positive
  • 3% asymptomatically secrete
  • Partially protected against by HSV1 antibodies
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35
Q

What are the innate defences against HSV? What is the role of interferon?

A
  • Induced by epithelium infection
    1. Infected epithelial cells make IFNβ
    1. PAMP-PRR interactions induce macrophages and DCs to make cytokines (IFNα)
    1. Type 1 interferons (IFNα/β) protect uninfected cells from virus infection and induce influx/activation of NK cells
    1. NK cells recognises and bind HSV infected cells, lysis
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36
Q

What are the adaptive responses against HSV?

A
  • T cells important (4 and 8)
  • CD4 for helping and activating CD8
  • CD8

o Controls HSV replication in skin/mucous/ganglia

o ICP47 production inhibits MHC I presentation and expression

o Specific HSV CD8 found clustered around ganglia without damaging neuron (maintain but don’t control infection)

o Genital lesions: CD8 migration linked with viral clearance

  • B cells
  • Limited efficiency of antibodies in HSV protection
  • Maternal abs can protect against neonatal infection
  • Don’t play role as large as T cells
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37
Q

Are B or T cells more important for controlling HSV infection? Why?

A
  • T cells
  • Antibodies induced by experimental vaccines not associated with protection
  • Antibody deficient patients don’t have worse recurrences
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38
Q

Why can’t HSV be eliminated permanently? Is this true for infections of epithelial cells and neurons?

A

• Eventually can eliminate in epithelial cells

o Complement, NK cells, T cells (but delayed because of ICP47)

o Lyse infected cells

• Neurons virus persists

o Limited production of viral proteins (episomal state)

o Low levels of neuron MHC I expression

o ICP47 inhibits peptide transport to MHC I

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39
Q

How can HSV be diagnosed?

A
  • Grow virus, look for antigens or nucleic acids, look for antibodies
  • Can determine if new or recurrent latent infection
40
Q

What are the phases of HSV infection?

A

• Acute Phase

o Primary infection

o Lots of antigen, fair amount of agent, growing levels of antibodies (IgM, IgG)

o More likely to transmit during primary infection because high viral load

• Latent Phase

o Reactivations

o Less antigen

o Less agent

o Lots of antibodies (total specific serum antibody, IgG, IgM)

41
Q

How can HSV be treated? What is targeted?

A
  • Target DNA polymerase and NA synthesis
  • Acyclovir
42
Q

What is the action of acyclovir?

A
  • Guanosine/nucleoside analogue
  • No phosphate groups, lack 3’ OH so no DNA extension
  • Needs to be phosphorylated (pro-drug)
  • Active form has 3 phosphates
  • Binds DNA polymerase, inhibits viral DNA replication
  • Works in epithelial cells, not neurons
43
Q

How can HSV be controlled and managed?

A
  • No vaccines (need T and B cell response)
  • Antivirals (acyclovir, nucleoside analogues) but don’t remove latent infection
  • Physical barriers reduce spread (condoms, gloves)
  • But virus shed if symptomatic or asymptomatic
  • HSV2 associated with increased HIV transmission
44
Q

How many people have died from HIV? How many are currently infected?

A
  • 42.5 million deaths
  • 35.3 current infections
45
Q

What type of virus is HIV? What is its structure and what proteins are involved?

A
  • Retrovirus
  • Env Gene

o Glycoproteins (gp 120, gp 41)

o Envelope

• Gag Gene

o Matrix (p17)

o Capsid (p24)

o Nucleocapsid (p7)

• Pol Gene

o Reverse Transcriptase (p66, 51)

o Integrase (p32)

o Protease (p11)

  • RNA, 2 pieces
  • Lots of variability between gag, env proteins
  • Lots of diversity means can sustain genetic drift
46
Q

What is involved in HIV replication?

A

1 Fusion

  • Gp120 binds to CD4
  • Also uses co-receptor

2 Enter cell

• HIV RNA, RT, int, viral proteins

3 Viral DNA formed by reverse transcription

4 Viral DNA goes to nucleus integrates to host DNA (integrase)

5 New viral RNA used as genomic RNA and makes viral proteins

6 New viral RNA and proteins move to cell surface, form new immature HIV

7 Virus matures due to action of protease

47
Q

What are the stages of HIV infection?

A
  1. Primary infection
    * Lots of virus
  2. Clinical latency
  3. AIDS, disease stage

CD4+ T cells diminish over time

Lots of virus again at death

48
Q

How can HIV affect the GALT? What phase does this occur in?

A
  • . Primary infection
  • Galt destruction
  • Lose epithelial integrity
  • Lose tight junctions
  • More exposure to PRR interactions
  • T cells in gut are killed by HIV, lose activated and memory T cells
49
Q

What is virological set point? How does it arise and how is it measured?

A
  • Caused by vigorous immune response to HIV
  • Equilibrium between viral replication capacity and host anti-HIV defence
  • Measure with RT-PCR
  • Aim for undetectable viral load (<50copies/mL)
50
Q

How can HIV escape the immune system?

A
  • Very high viral mutation rate
  • Deletion of HIV specific CD4 T cells
  • Failure of specific antibody and CTL responses
  • Other mechanisms
51
Q

What impact does HIV have on the immune system?

A

• Neutrophils

o Recued bacteria killing

• B cells

o General ab increase

o Autoantibodies

o Poor vaccine response

o Reduced encapsulated bacteria killing

• T cells

o Less T cell help for B cells

o Less CTL for other viruses

• Macrophages

o Less phagocytosis

o Less chemotaxis

o Less killing

• NK cells

o Less function

• Aberrant immune response

o Immune activation leading to

o HIV replication

o Immune cell depletion

o Immune cell dysfunction

o Aberrant lymphocyte turnover

o Organ system dysfunction

52
Q

What influences the outcome of HIV infection?

A
  • Virus strain
  • Immune response
  • Other illnesses
53
Q

What can anti-retroviral therapies target?

A
  • Fusion/entry inhibitors
  • RT inhibitors
  • Integrase inhibitors
  • Protease inhibitors
54
Q

What are the benefits of combination therapy?

A
  • Target multiple areas at once
  • Synergistic potency/very active anti-retroviral therapy
  • Durable response
  • Minimises development of drug resistance
55
Q

What are ways to prevent HIV?

A
  • Treatment as prevention
  • Microbicides
  • Pre exposure prophylaxis
  • Circumcision
  • Prevent mum passing to child
  • Vaccine ideal, but difficult to make
56
Q

What unique properties of HIV make vaccine development difficult?

A
  • Natural immune response doesn’t control virus, protect from super-infection
  • Incomplete understood mechanisms of protection
  • High sequence diversity
  • Evade neutralising antibody response
  • Evade CTL and NK response
  • Want to achieve sterilising immunity
  • Latency and integration
57
Q

What would constitute an ideal HIV vaccine?

A
  • Prevent mucosal and parenteral transmission
  • No adverse reactions
  • Single dose
  • Long lived protection
  • Low cost
  • Stable, easy administration
  • Diverse protection
  • Therapeutic vaccines to replace therapy, prevent AIDS
  • Aim for Immune response (T cell, neutralising abs)
58
Q

Which immune responses would be most useful in a HIV vaccine?

A

• T cell

o CD8/CTL to kill infected cells

o CD4+ helpers

o Often only partial clearance

o Could silence HIV

• Broad neutralising antibodies

o Prevent transmission potentially

o But readily avoided by sequence variation in envelope

59
Q

What are features of broad neutralising antibodies?

A
  • Neutralising abs bind to structure trimers (3 gp120)
  • Non-neutralising bind to highly immunogenic inner face of gp120 monomers
  • Important to target envelope
  • Broad neutralising antibodies characteristics

o Long regions

 Abs bind HIV

 Antibody combining regions

 Abs with long combining regions often eliminated by tolerance mechanisms

o Excess accumulation of somatic mutations

 Unusual because often eliminated by tolerance deletion

o Self-reactive with host molecules in addition to reacting with HIV envelope

 Self-reactive antibodies often eliminated by tolerance deletion

60
Q

What are possible HIV vaccine development strategies’? What are the features and issues?

A

• Dead protein

o Envelope subunit, vlps, whole inactivated virus

o Not good efficacy

• Live attenuated virus

o Safety issues

• Genetically engineered live virus

o Most promising

o Use virus that can express viral protein (e.g. adenovirus)

o E.g. RV144 Vaccine (31% efficacy)

61
Q

What were findings from the RV144 vaccine?

A
  • Doesn’t impact viral load
  • Can potentially protect from infection
  • Limited primary neutralising ab
  • Limited CD8 T cell immunity
  • Other immune effectors may have role
  • Greatest protection if early and low risk
  • Need to consider variables

o Mode of transmission

o Exposure frequency

o Vaccine vector immunity

62
Q

What are the features of papillomaviruses? Which genotypes affect man?

A

• Small ds DNA

o Closed circular genome

  • Species specific
  • Replicate in skin only
  • Site specific
  • Warts
  • Cancers
  • Don’t grow in cell culture
  • 100 different genotypes

o Cutaneous warts – HPV 1, 2

o Genital warts – HPV 6, 11

o Genital cancers – HPV 16, 18 o EV/Epidermodysplasia Verruciformis – HPV 5, 8

63
Q

What is the significance of HPV?

A
  • Incidence faster increase than herpes past 3 decades
  • Only second to chlamydia or most common STD
  • 79% of women may get it
  • Can be asymptomatic
  • Can be transient
64
Q

How does HPV spread? Is the blood involved?

A
  • Particles on warts
  • Direct skin to skin contact
  • Virus doesn’t use blood at all
  • Enter skin through scratches/micro-abrasions
  • Mucus membrane likely to be infected
  • Micro-abrasions happen during sex, mucus environment, easy spread
65
Q

What is the process of HPV invasion?

A
  1. Enters at basal layer

• Area where lots of cell division

  1. Produce early proteins (E2), viral genome exists as episome
  • E2 protein links episome to chromosome DNA so virus can replicate when cell replicates
  • Episome doesn’t integrate to host DNA
  • PV non lytic
  1. Cell replication enhanced
  • E6 and E7 proteins
  • Bind to cellular proteins that control cell division
  1. Multiple copies of episome made in each cell

• Episome transported to upper layers

  1. Late proteins and E4 made, viral genomes packaged to virions
  • Capsid proteins L1 and L2 made in cells which have differentiated into keratinocytes
  • Form non replicating barrier layer of skin
  1. Virus filled keratinocytes shed from surface
66
Q

What are the roles of E2, E4, E6 and E7?

A
  • E2 protein links episome to chromosome DNA so virus can replicate when cell replicates
  • E2 usually negatively represses E6 and E7 transcription
  • E4 as structural protein
  • E6 and E7 proteins bind to cellular proteins that control cell division (enhance it)
67
Q

What are features of HPV infection?

A
  • Virus only shed from skin surface
  • No viral antigen secreted from cells
  • Virus not blood borne
  • Infections doesn’t result in dead cells
68
Q

How does the immune system react to HPV?

A

• Poor induction

o Little/no viral antigen goes to lymph nodes

o Little/no antigen taken up by skin DCs

o No inflammation to activate DCs to migrate to lymph nodes

• Weak and late response

o Antibodies to L1, L2 (capsid proteins)

 Happens late (HPV16) or never (HPV6)

 Protective, not therapeutic

 Ab recognises conformation dependent epitopes on structural proteins

o Antibodies to early proteins

 Predominantly E7

 Associated with invasive HPV16

• Cell mediated immunity

o People with EV often have cell mediated immune defect and low helper T cell function

69
Q

What kinds of vaccines are needed against HPV?

A
  • Therapeutic treat warts
  • Prophylactic prevent HPV
  • Therapeutic for cervical cancer
70
Q

What are the current methods for treating warts?

A
  • Burn, poison, freeze, cut
  • Immunotherapy: interferon, Imiquimod (TLR7 ligand)
71
Q

What is the basis of using VLPs in a PV vaccine?

A
  • Recombinant L1 protein, in eukaryotes, assemble to capsids look like virions, enter cells like virions
  • Induce virus-neutralising antibody and cell mediated response (wouldn’t see T cells in infection site without immunisation)
72
Q

What are features of the GPV Gardasil vaccine? • PV immunogenic due to capsid proteins (L1)

A
  • VLPs mimic PV capsids, induce PV neutralising antibody
  • Highly successful
  • Intramuscular, 3 shots
  • But can’t guarantee efficacy against strains not in vaccine
73
Q

What are the challenges facing HPV vaccines?

A
  • >100 HPV genotypes (40 infect anogenital epithelium)
  • Mother to child transmission
  • Length of protection at mucosal surfaces
  • Vaccinate men? Anal cancer
  • Possible eradication
74
Q

What is the significance of cervical cancer?

A
  • HPV infection →cervical dysplasia → cervical cancer
  • Per year: 500000 new cases, 240000 deaths
75
Q

What are koilocytes? What do they indicate?

A

• Pap smears show peri-nuclear cytoplasmic vacuolization (koilocytosis), indicates HPV infection

76
Q

What are the levels of cervical intraepithelial dysplasia?

A
  • Normal
  • Mild (few abnormal cells)
  • Moderate (abnormal cells in half of layer)
  • Severe (abnormal cells in entire layer)
  • Invasive cancer (abnormal cells beyond basement membrane)
77
Q

What causes PV to lead to cancer?

A
    1. HPV DNA randomly integrated into host DNA (not episome)
    1. Loss of several HPV genes
    1. If lose E2, cancer can grow because E2 usually negatively represses E6 and E7 transcription
    1. E6 and E7 proteins expressed

o E6 interacts with p53

o E7 interacts with Rb

• Cell cycle usually tightly regulated

78
Q

What are the normal roles of Rb and p53 and which PV proteins interact with them?

A

Rb

  • Controls G1 to S transition
  • When active, associates with E2F and halts cell cycle
  • Bound by E7

P53

  • Cause cell growth to stop and apoptosis to repair damage
  • More than 50% of human cancers have p53 mutation
  • Bound by E6
79
Q

How can cells expressing E6 and E7 be cleared?

A

• Can use cytotoxic lymphocytes to clear cells expressing E6 and E7

80
Q

What are the ideas and challenges for cervical cancer vaccines?

A
  • Keratinocytes relatively resistant to killing by cytotoxic T cells
  • Problems with antigen presentation
  • Which PV protein, which delivery system?
  • How long would it last • Immunotherapy and resistance
  • Target E7

o Therapeutic vaccines

81
Q

What can result from local and systemic syndromes as a result of STIs?

A

Local (mostly urogenic)

  • Lesions
  • Urethritis, vaginitis, cervicitis, proctitis, pharyngitis
  • PID

Systemic

  • HIV AIDs
  • Syphilis (primary, secondary, tertiary, congenital)
82
Q

What are some ways to diagnose STIs?

A

Clinical history

  • Swabs
  • Microscopy
  • Culture
  • Antigen detection
  • Nucleic acid amplification based detection

Blood Tests

  • Antibody detection
  • Antigen detection
  • Viral culture
  • Viral load testing
83
Q

How does STI treatment differ between what is ideal and the reality?

A

Ideal

  • Based on clinical syndrome
  • On the spot
  • Single dose
  • Effective
  • No side effects
  • Cheap
  • Efficient partner treatment
  • Effective Prevention

Reality

  • May be asymptomatic
  • Diagnosis may be unclear without test
  • Longer courses of treatment
  • Antibiotic resistance
  • Recurrent infections
  • Multiple infections
  • Unknown, undisclosed, reluctant partners
  • Prevention can fail
84
Q

What is the reproductive rate? What do different RO values represent?

A
  • Measure of biological success of an organisms
  • Average number of secondary cases of infection produced by ONE primary case in completely susceptible population
  • RO > 1 = epidemic (spread, increasing cases)
  • RO = 1 = endemic
  • RO < 1 = disease eventually disappears
  • RO = βcd
  • β = transmissibility
  • c = number of contacts while infections o
  • d = duration of infectivity
85
Q

What is an important influence for RO when considering STIs?

A

• For STIs, RO heavily influenced by average rate of acquisition of new sexual partners

86
Q

How do disease and reduced transmission differ?

A
  • Disease Transmission = some infections cause others to progress to disease (e.g. 1 in 10)
  • Reduced Transmission = fewer secondary infections, no subsequent cases
87
Q

What can influence disease transmissibility (β)?

A
  • Reduce with condoms
  • Influenced by other STIs (screening, treatment, lower transmission)
88
Q

What can influence the duration of infectivity (d)?

A

• Influenced by treatment

89
Q

What can influence the number of contacts while infectious (c)?

A

• Influenced with core group interventions, community wide behavioural change

90
Q

What makes up a sexual network?

A

Core transmitters

  • Highest prevalence

Bridging population

  • Moderate prevalence

General population

  • Lowest prevalence
91
Q

In what ways are STIs managed in Australia?

A
  • Public awareness
  • Prompt, confidential diagnosis and treatment (GPs, Specialist clinics, remote heath services)
  • Partner tracing and treatment
  • Screening
  • Vaccination
  • Surveillance

o Diagnoses

o Antimicrobial resistance

o Behaviour

• Safe sex promotion

92
Q

What are features of STIs in remote Australia?

A
  • Higher rates
  • More likely to see uncommon STIs
  • More likely to see common STIs with uncommon features
  • Similar HIV prevalence (but risk higher due to prevalence of other STIs)
  • Obstacles for treatment (access to care, partner tracing)
93
Q

How could chlamydia be controlled?

A
  • Surveillance (prevalence, incidence, trends over time)
  • Targeted screening if high risk
  • Educate health care professionals
  • More community awareness
  • Better partner notification processes
94
Q

What trends and features exist for chlamydia, gonorrhoea, syphilis and HIV?

A

Chlamydia

  • More females
  • General increase, small decrease lately
  • Most susceptible = 15-24
  • Not enough people tested (tip of iceberg)

Gonorrhoea

  • More men (particularly men who have sex with men)
  • Increase lately (issue for risk of other STIs and HIV)
  • Need to monitor resistance patterns

Syphilis

  • More men (MSM)
  • Slightly increasing now

HIV

  • Slight increase now
  • Most newly diagnosed = MSM
  • Most newly acquired = MSM
95
Q

How might HIV be controlled?

A
  • Surveillance, epidemiology
  • Testing, counselling
  • Health promotion (gay, people with HIV, injection drug users, sex workers/clients, aboriginal, travellers to/from countries with high prevalence, sexually active young people)
  • Treatment, care, support
  • Issues for legal and discrimination
  • Coordination, management, monitoring, evaluation

Second Year Microbiology (8 decks)

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