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Microbiology 2 > STIs > Flashcards

STIs Flashcards

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1
Q

what are STIs?

A

diseases intimately linked to human behaviour, both social and sexual

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2
Q

why can STIs be controlled more than other infectious diseases?

A

they can be prevented from spreading via use of barrier methods and education in comparison to respiratory diseases

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3
Q

what 3 reasons are there for STI incidence increasing?

A
  1. Use of the pill since the 1950s has replaced barrier methods of contraception that help prevent spread of STIs.
  2. Change in public attitudes to sex – increased numbers of sexual partners in many western countries has occurred in the last several decades. Now driven by widespread internet use and dating apps
  3. Other factors: Problems of drug-resistant strains of bacteria, poor attendance at STI clinics by some infected individuals, lack of appropriate sex education advice etc
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4
Q

what viruses can cause STIs?

A
  • Papilloma virus = Genital warts
  • Herpes simplex virus 2 = Genital herpes
  • Hepatitis A, B and C = Hepatitis, liver cancer
  • HIV = AIDS
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5
Q

what bacteria can cause STIs?

A
  • Chlamydia trachomatis = Urethritis, cervicitis, LGV
  • Neisseria gonorrhoeae = Gonorrhoea
  • Treponema pallidum = Syphilis
  • Heamophilus ducreyi = Chancroid
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6
Q

what fungi can cause STIs?

A

candida albicans = thrush

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7
Q

what protozoa can cause STIs?

A

Thrichomonas vaginalis = vaginitis

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8
Q

what bacteria cause gonorrhoea?

A

Neisseria gonorrhoeae

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9
Q

what bacteria cause syphilis?

A

Treponema pallidum

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10
Q

what bacteria cause chlamydia?

A

Chlamydia trachomatis

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11
Q

what do the bacteria that cause gonorrhoea, syphilis and chlamydia have in common?

A
  • All of these bacteria are highly host-adapted strict pathogens and cannot survive long outside the human body
  • they are spread directly from person to person with no animal reservoir
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12
Q

what are Neisseria gonorrhoeae?

A
  • Gram-negative coccus, characteristically seen as diplococci in samples of discharge
  • Non-motile
  • Humans are the only host: No animal reservoir
  • Transmission is directly from person-person
  • Poor survival outside the human host but can be grown in pure culture
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13
Q

how is Neisseria gonorrhoeae spread?

A

Spread via intimate mucosal contact is needed for transmission, usually via the vagina, or the urethral mucosa of the penis.
- However, various sexual practices can result in infection of the throat or the rectal mucosa

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14
Q

what are the symptoms of gonorrhoea?

A

Symptoms usually appear 2-7 days post-infection
- Male: Thick urethral discharge, pain on urination
- Female: vaginal discharge
- Up to 50% of infected females may be asymptomatic or only have mild initial symptoms

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15
Q

why is the asymptomatic expression of gonorrhoea so dangerous in women?

A

If women are asymptomatic and don’t seek treatment, can lead to serious complications:
- Pelvic Inflammatory Disease (PID)
- Damage to fallopian tubes, leading to infertility
- Other disseminated symptoms
- In pregnancy, can be passed to the baby during birth, where the bacterium colonises the eyes, leading to blindness if not treated

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16
Q

what virulence factors does Neisseria gonorrhoeae use during infection?

A
  • pili
  • protein II (PII/Opa)
  • capsule (polysaccharide)
  • protein I (PI)
  • IgA protease
  • Tbp/Lbp
  • LPS/LOS
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17
Q

how do Neisseria gonorrhoeae initally attach to mucosal surfaces and epithelia?

A
  • Many surface proteins and structures of the cell are virulence factors, involved in adhesion and invasion of the epithelial cells lining the urethra or vagina.
  • Good adhesion is essential for a mucosal pathogen in this environment to prevent being dislodged by urine flow.
  • Initial attachment to epithelial surface by long-range pili which stick from cell surface
  • Outer-membrane proteins intimately attach bacteria to mucosal surface e.g. Protein II/Opa
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18
Q

what is the role of the capsule for Neisseria gonorrhoeae?

A

the polysaccharide capsule resists phagocytosis and screens immunogenic epitopes from B cells in order to avoid detection

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19
Q

what is the role of protein I for Neisseria gonorrhoeae?

A

Protein I is an outer membrane protein which enables the bacteria to survive phagocytosis

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20
Q

what is the role of the IgA protease of Neisseria gonorrhoeae?

A

IgA protease is secreted by the bacterium to inhibit opsonisation by complement

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21
Q

what is the role of Tbp/Lbp in Neisseria gonorrhoeae?

A

Transferrin/lactoferrin binding-proteins to scavenge iron for nutrition

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22
Q

what is the role of LPS/LOS in Neisseria gonorrhoeae infection?

A

Lipopolysaccharide induces inflammation at infection site, leading to pain

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23
Q

what are the 2 ways in which Neisseria gonorrhoeae evade the immune response?

A
  1. The LPS can be modified by attaching sialic acid residues to it (sialylation) so that it “looks” like host tissue to the immune system and so does not provoke an immune response.
    - Sialic acid is common in mammalian modifications, not common in bacteria
    - This is “molecular mimicry”.
  2. Many of the surface proteins (e.g. pilin PilE and PII) are highly immunogenic, but gonococci can continuously produce sequence variants that make it difficult for the immune system to mount an effective response.
    - Such proteins represent hypervariable surface antigens that allow immune evasion.
    - This is “antigenic variation”
24
Q

what is an example of antigenic variation in Neisseria gonorrhoeae?

A

pilin (PilE) variation

25
Q

what is PilE?

A
  • PilE is the main gene that encodes pilin subunit
  • In the pilin subunit, the N-terminus is highly conserved to build the pilin structure/fibre
  • The outside of the fibre is variable region which can be detected by T cells/antibodies
26
Q

how does Neisseria gonorrhoeae undergo antigenic variation of PilE?

A

N. gonorroheae can swap out the variable region of the gene in a recombinase-dependent manner during growth
- Partial sequence homology between the silent pilS loci and the expressed pilE gene allows RecA-mediated recombination to occur, giving rise to a novel pilE variant protein, by “gene conversion”
- Constantly mixing and matching the silent genes, then incorporating into variable region
- The pilin will still be functional, but less recognizable by host immune system

27
Q

why is antigenic variation of pilin useful for Neisseria gonorrhoeae?

A
  • Population of N. gonorroheae cells inoculated from a single colony, genetically identical/clonal, and then you sequence the variable region of the pilin, they will all have different sequences
  • This means host immune cells cannot recognise all the cells in the population due to antigenic variation
28
Q

what is the epidemiology of Neisseria gonorrhoeae?

A
  • Asymptomatic carriers are major reservoirs of infection in the human population (up to 50% of females, and 10% of males)
  • Tracing and treatment of sexual contacts of infected symptomatic individuals is important in preventing spread
29
Q

what treatments have been and are available for Neisseria gonorrhoeae?

A
  • 1940s -1970s: Penicillin, but resistance became a major problem
  • 1980s: Fluoroquinolones, e.g. ciprofloxacin (DNA gyrase inhibitor) - resistance now a major issue so they cannot be used, DNA gyrase can undergo point mutations so quinolones are redundant
  • 2000s – present: Cephalosporins, e.g. ceftriaxone and cefixime - resistance is becoming quite common
30
Q

what major problem is on the rise relating to Neisseria gonorrhoeae?

A

multi-drug resistant gonorrohea – there is a real possibility this may become an untreatable disease

31
Q

what are spirochetes and give examples:

A

Flagellum is within the periplasmic space, and bacterium is spiral in shape
- T. pallidum is a spirochaete causing syphilis
- Borrelia can cause Lyme disease – tick borne zoonosis causing infectious arthritis
- Leptospira cause leptospirosis (Weil’s disease), transmitted through rat urine or faeces

32
Q

what is syphilis?

A
  • A complex disease, first described in Europe in the 1400s.
  • Its symptoms can be varied and easily confused with other diseases, making traditional diagnosis difficult (“The Great Imitator”)
  • Caused by the spirochaete Treponema pallidum, discovered in 1905
  • Infection is CHRONIC and in untreated cases may last decades, with maybe 30-50% mortality.
  • The disease progresses in different stages
33
Q

what is Treponema pallidum?

A
  • spirochete bacteria
  • very fragile
  • slow growing
  • poor survival outside the host
34
Q

what does Treponema pallidum infection require?

A

Infection requires intimate sexual contact, and is aided by minute tissue abrasions that occur during sex

35
Q

what are the different stages of syphilis?

A

primary
secondary
latent
tertiary

36
Q

what is the primary infection of syphilis?

A
  • Initial infection presents as chancre sores on penis/vagina/anus
  • Short-lived
  • Some patients who notice the sores won’t seek diagnosis/treatment
  • Primary infection will either lead to secondary/systemic infection or latent infection
37
Q

what is secondary/systemic infection of syphilis?

A
  • systemic infection including rash, fever, neurological symptoms
  • neuro-syphilis can be fatal
  • these harsher symptoms occur < 1 year
  • after this infection, the illness resorts to latent infection
38
Q

what is latent infection of syphilis?

A

there are no symptoms expressed
- the bacteria resides in the body and can reactivate back to systemic/tertiary infection 5-50 years later
- 30% with latent infection will progress to the severe syphilis infection

39
Q

what is the tertiary/systemic infection of syphilis?

A

5-50 years later, infection progresses to nasty systemic infection of bones, cardiac tissue, nerve disease
- Affects brain – patients are neurologically disturbed
- Patients develop Gumma: a nodule or tumour-like growth in organs
- At this point 50% patients die
- 30% with latent infection will progress to the severe syphilis infection

40
Q

why is syphilis tricky to diagnose?

A
  • as there are so many wide-ranging symptoms
41
Q

what virulence factors does Treponema pallidum use to survive in the host long term?

A
  1. lack of endotoxins and exotoxins
  2. invasion of immune-privileged tissues
  3. ability to maintain infection with few organisms
  4. lack of surface antigens
  5. low iron requirements - can obtain sequestered iron
42
Q

how does lack of endo- and exotoxins help Treponema pallidum survive in the host long term?

A

Lack of endo- and exotoxins:
- T. pallidum lacks LPS, the endotoxin found in the outer membranes of many Gram-negative bacteria, so doesn’t have MAMPs that are instantly recognised by the immune system
- The attachment of T. pallidum to cells does not harm the cells
- This indicates that cytolytic enzymes or other cytotoxins most probably do not play a role in syphilis pathogenesis.

43
Q

how does invasion of immune-privileged tissues help Treponema pallidum survive in the host long term?

A

Invasion of “immune-privileged” tissues:
- T. pallidum penetrates a broad variety of tissues, including so-called “immune privileged”: the central nervous system, eye, and placenta, where there is less surveillance by the host’s innate immune system.

44
Q

how does Treponema pallidum’s ability to maintain infection with few organisms allow it to survive long term in the host?

A

Ability to maintain infection with few organisms:
- T. pallidum may also exploit its slow growth to survive in tissues, even those that are not immune privileged.
- By maintaining infection with very few organisms in anatomical sites distant from one another, T. pallidum may prevent its clearance by failing to trigger the host’s immune response, which was may require a “critical antigenic mass”.

45
Q

how does lack of surface antigens help T. pallidum survive in the host long term?

A

Lack of surface antigens:
- One of most prominent features of T. pallidum is that it has only rare integral proteins in its outer membrane, approximately 1% of the number found in the outer membrane of E. coli.
- However, these rare proteins are likely to be very important in interactions with the host; for this reason, their identity has been the subject of intense research.

46
Q

how does T. pallidum’s low iron requirements enable it to survive in the host long term?

A

Low iron requirements, ability to obtain sequestered iron:
- T. pallidum may be able to acquire iron from host proteins.
- It may also overcome the iron sequestration problem by using enzymes that need metals other than iron as their cofactors.
- In addition it lacks an electron transport chain, which is made up of enzymes that use iron as a cofactor, which decreases its overall demand for iron

47
Q

how was syphilis historically treated?

A

In 1910 Paul Ehrlich developed salvarsan – an organic arsenic-containing drug which was partially effective but quite toxic

48
Q

what is the current treatment of syphilis?

A

0 T. pallidum is very sensitive to penicillin, which is still the best treatment, as little resistance has developed.
- Its introduction in the 1940s led to a massive reduction in the numbers of cases and the disease became rare.
- However, because the bacterium is so slow growing it is essential that a high level of penicillin is maintained in the body for several weeks; it must be injected either daily IV or 2x injections of a slow release formulation in the buttocks over a 1 month period (painful!)
- Not everyone follows through with the treatment

49
Q

what is the epidemiology of syphilis?

A

In the 1970s numbers of cases started to rise again; it is now a significant STI.
- A particular problem is co-infection of syphilis and HIV – infection with syphilis makes it several times more likely that HIV infection occurs

50
Q

what are Chlamydia bacteria?

A

Chlamydia are small gram-negative wall-less bacteria which are obligate intracellular parasites:
- Cannot survive outside of mammalian host cell – cant be cultured on agar in lab
- Tiny genome – genome reduction means it is dependent on host for common cell processes - like a virus

51
Q

what is the life cycle of chlamydia?

A

They have a complex life-cycle based on two functionally distinct cell forms:
- “Elementary body” (EB) – survives outside of host cells and initiates infection
- “Reticulate body” (RB) – Differentiates from the EB and is responsible for intracellular growth

52
Q

which Chlamydia species causes an STI?

A

Chlamydia trachomatis causes STIs, but only certain serovars:
- A, B, C - cause Trachoma – a serious eye infection
- D,K – cause Urethritis (men) and Cervicitis (women) - STI
- L1-L3 – cause Lymphogranuloma venereum (LGV) – STI

53
Q

what are the symptoms of Chlamydia in men?

A
  • Thin, watery urethral discharge
  • Sometimes pain on urination
  • Can be asymptomatic
54
Q

what are the symptoms of Chlamydia in women?

A
  • Infection of the cervix
  • Urethritis
  • Infertility and ectopic pregnancy
  • Very often asymptomatic
55
Q

why are screening programmes important in tackling Chlamydia?

A

Screening programmes are important because of the often asymptomatic nature of the infections

56
Q

how can Chlamydia be treated?

A
  • Chlamydia are insensitive to beta-lactam, cephalosporin and vancomycin antibiotics as they have no peptidoglycan cell wall.
  • Have to use alternatives like Tetracycline/doxycycline or Azithromycin, which have some side-effects

Microbiology 2 (10 decks)

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