STIs

Question 1

features of bacterial STIs

Answer 1

• highly infectious
• only in humans
• don’t survive well outside host
• can be asymptomatic

Question 2

Chlamydia gram stain

Answer 2

gram negative

Question 3

Chlamydia life cycle

Answer 3

1. elementary body (EB) - infectious stage

2. reticulate body (RB) - replicative stage

Question 4

Chlamydia pathenogenesis

Answer 4

• inflammatory response

- hsp60 can induce chronic inflammation

Question 5

Chlamydia diagnosis

Answer 5

• PCR of samples
• EIA
• cannot grow on plate (need host cell)

Question 6

Chlamydia treatment

Answer 6

antimicrobials that target RBs, and stay active for a while due to long life cycle

Question 7

Gonorrhoea gram stain

Answer 7

gram negative diplococcus

Question 8

Gonorrhoea pathenogenesis

Answer 8

1. adhesion attachment
2. spreads in muscosal secretions
3. trigger inflammatory response

Question 9

Gonorrhoea diagnosis

Answer 9

• gram stain of specimen
• PCR
• culture on selective enriched medium with antibiotics and 5% CO2

Question 10

Gonorrhoea treatment

Answer 10

antibiotics (however gonorrhoea is highly resistant)

Question 11

Syphilis gram stain

Answer 11

gram negative spiral rod

Question 12

Syphilis pathenogenesis

Answer 12

1. infection: 3 week incubation
2. primary syphilis: contagious ulcer or asymptomatic
3. secondary syphilis: contagious rash, lesions, warts
4. tertiary syphilis: targets eyes, ears, heart & brain

Question 13

Syphilis diagnosis

Answer 13

• PCR
• dark ground microscopy
• rapid plasma reagin test (RPR)

Question 14

Syphilis treatment

Answer 14

penicillin

Question 15

Human papilloma virus (HPV) structure

Answer 15

non-enveloped dsDNA, with L1 & L2 capsid

Question 16

HPV entry, replication & transmission

Answer 16

1. enter basal layer of skin (via microabrasions)
2. E2 links viral episome to mitotic chromosomes
3. E6/E7 enhances cell replication
4. E4 package viral genome into virion
5. virus filled keratinocytes sloughed off via skin-to-skin contact

Question 17

HPV immune response

Answer 17

• weak and late immune response
• antibodies for L1 & L2 capsid proteins
• antibodies for E7 (and E2)

Question 18

cervical cancer

Answer 18

1. HPV can lead to cervical intraepithelial dysplasia
2. CIN 1-3: level of abnormal cells within epithelium that must be treated
3. if not treated, abnormal cells migrate beyond basement membrane - invasive cancer

Question 19

retinobalstoma susceptibility gene (Rb)

Answer 19

• stops transition from G1 to S phase

- pauses DNA synthesis by inhibiting E2F transcription factors

Question 20

p53 gene

Answer 20

transcription factor that initiates apoptosis due to DNA damage

Question 21

E6 & E7 function

Answer 21

inhibit Rb & p53, therefore inhibits pausing cell cycle and apoptosis

Question 22

E2 fucntion

Answer 22

stops transcription of E6 & E7, it is lost during HPV integration into host genome

Question 23

HPV vaccine

Answer 23

• treats warts (primary & secondary infections)
• treats CIN 1,2,3
• prevents HPV infection

Question 24

HPV treatment

Answer 24

• vaccine (Gardisil - VLPs)
• interferon (anti-viral cytokine)
• topical application of immune enhancing drug

Question 25

Herpesvirus (HSV) structure

Answer 25

enveloped dsDNA HSV 1 serotype: above waist, spread by saliva HSV 2 serotype: below waist

Question 26

HSV transmission & entry

Answer 26

1. glycoproteins of enevelope bind to cell surface receptors | 2. binding triggers fusion of membranes and release of capsid

Question 27

HSV latency

Answer 27

spread from epithelial cells to dorsal root ganglia

Question 28

HSV treatment

Answer 28

acyclovir antiviral inhibits viral DNA replication

Question 29

HIV structure

Answer 29

enveloped two copies of positive sense ssRNA

Question 30

HIV virion components

Answer 30

- envelope proteins - gag proteins: capsid & matrix - pol proteins: reverse transcriptase, integrase, protease

Question 31

HIV pathenogenesis

Answer 31

- high viral mutation rate - deletion of HIV CD4+ T cells - inactivation of HIV antibodies

Question 32

HIV immune response

Answer 32

- autoantibodies - poor response to vaccines - decreased T helper cells for B cell activation - decreased macrophages, NK cells & cytotoxic T cells - AIDs

Question 33

HIV treatment

Answer 33

- integrase, protease, reverse transcriptase inhibitors | - HAART (highly active anti-retroviral therapy)