Lec 33 - STIs Flashcards

1
Q

Why is there more opportunity to control STIs rather than other diseases eg respiratory diseases

A
  • STIs linked to social and sexual behaviour rather than just biology
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2
Q

Why are we experiencing a rise in STIs in recent years?

A
  • introduction of the pill has removed use of barrier methods for protection against STIs eg condoms
  • attitudes towards sex has changed - more sex and increased use of dating apps
  • rise of resistant strains of STIs
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3
Q

Give 5 examples of STIs and state their cause

A
  1. HIV - AIDS
  2. Hep A/B/C - Hepatits (both viral)
  3. Chlamydia trachomatis - Chlamydia
  4. Trepomona pallidum - Syphillis
  5. Neiserria gonorrhoae - Gonorrhoae
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4
Q

What type of pathogen are bacterial STIs? Describe what this means

A
  • STRICT
  • highly adapted to the host
  • person;person spread w/ no animal resevoir
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5
Q

Give the name of bacteria that causes Gonorrhoea and state its structure when observed in discharge

A
  • Neisseria gonorrhoea*
  • Gram -ve coccus, high proportions of diploccoci
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6
Q

How is Neisseria gonorrhoea transmitted and can it be grown in pure culture?

A
  • transmitted through intimate mucosal contact eg vagina and urethral mucosa (of penis)
  • yes it can be grown in pure culture although does not survive well outside of the host
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7
Q

What are the symptoms of gonorrhoea?

A
  • males - thick dischagre, pain on urination
  • females - vaginal discharge
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8
Q

What are the problems that can arise because of the fact that 50% of females are asymptomatic?

A
  • damage to the fallopian tubes leading to infertility
  • during pregnancy, N. gonorrhoea can colonise the eyes leading to blindness
  • because of the high proportion of asymptomatics need to contact sexual partners of symptomatics to prevent spread
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9
Q

Give 4 examples of the VFs found in N. gonorrhoea

A
  1. capsule - resist phagocytosis
  2. pili and Protein II - adhering to the host cells
  3. IgA protease - breakdown secretory IgA
  4. Tbp/Lbp - acquire Fe from host cell
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10
Q

How does N. gonorrhoea evade the immune system?

A

MOLECULAR MIMICRY

  • sialylation of LPS residues prevents immune response because makes it look like host cells

ANTIGENIC VARIATION

  • phase variation and differential antigenic expression means that the immune system cannot provide an effective response
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11
Q

Give an example of antigenic variation in N. gonorrhoea

A

Differing the pilin proteins expressed on the surface because they are immunogenic. PilE normally expressed but RecA mediated recombination between pilE and pilS (silent loci) can create variants

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12
Q

What antibiotics can be used to treat gonorrhoea and what is a mjor problem associated with the disease currently?

A
  • both penicillin and fluoroquinolones have been used in the past however HIGH levels of resistance now
  • cephalosporins used - however increasing resistance
  • major problem = multi drug resistant strains now exist. looking v real that we will have untreatable gonorrhoea
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13
Q

What bacteria causes Syphillis?

A

Treponema pallidum

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14
Q

What phylum does Trepomponas pallidum belong and what is its main feature?

A
  • Spirochaetes
  • has a flagellum within the periplasm - helps to rotate the whole cell so can swim through mucus etc
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15
Q

How is syphillis passed on ?

A
  • intimate sexual contact
  • require minor tissue adrasions that occur during sex
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16
Q

Draw a diagram that illustrates the lifecycle of Trepomponas pallidum and at each stage list the symptoms

A
17
Q

List the 5 main ways that T. pallidum can survive in the host long-term

A
  1. lack of surface proteins / antigens - 1% that of E. coli and only integral protein may play a major role in attachment to host?
  2. few organisms required to establish infection - due to the SLOW growth of T. pallidum only a few organisms at distant sites required theefore critical antigenic mass is not reahed to stimulate immune system
  3. lack of endotoxin/LPS therefore doesnt stimulate IR. also when attached to cells do not kill them sugesting no cytolytic enzymes released
  4. invade immune privilidged cells eg CNS, eye, placenta
  5. low requirement for Fe/can obtain from cells - lack of Fe containing enzymes (use other metal ion cofactors) , no ETC (which uses Fe based enzymes)
18
Q

What feature of T. pallidum means that is causes CHRONIC infection

A

slow growing

19
Q

Describe the treatment of Trepomponas pallidum

A

due to slow growing nature, high doses of penicillin need to be given for a few weeks

daily injections of IV penicillin

20
Q

What disease is also correlated to syphillus infection?

A

co infection with HIV

21
Q

Describe Chlamydia and state the bacteria that causes it

A
  • Chlamydia trachomatis
  • wall-less obligate, intracellular parasite
22
Q

Draw a diagram to illustrate chlamydia life cycle and describe the 2 forms that exist

A

EB - ELEMENTARY BODY - required for survival outside of cellsand invovled in invasion

RB - RETICULATE BODY - intracellular growth

23
Q

Do all serovars of Chlamydia result in STIs?

A

no, only strains D/K result in STIs - urethritis (men) & cervicitis (women)

24
Q

Describe the symptoms of chlamydia is men and women

A

men - thin watery dischagre, pain on urination

women - cervisitis, urethra infection, infertility & ectopic pregnancy

25
Q

how is chlamydia treated?

A

because no peptidoglycan, B lactams do not work therefore need tetraclycine/doxycycline - side effects