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Unit 8 > Pathogens V: Sexual health and STIs > Flashcards

Pathogens V: Sexual health and STIs Flashcards

1
Q

What service caters for sexual health problems?

A
  • Combined sexual health clinics
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2
Q

What 5 things should a sexual health service provide?

A

1- Accessibility: local combined sexual health clinics
2- Confidentiality: just need contact number
3- Efficiency: >98% are seen within 2 working days
4- Open-mindedness
5- Positivity

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3
Q

What are the big 5 sexually transmitted infections? What is their causative organism?

A

*All can be present without clinical symptoms

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4
Q

What are the main viruses that cause STI?

A
  • Human herpes (Human herpes virus)
  • Anogenital warts (Human papillomavirus)
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5
Q

What are the main bacterial causes of STI?

A
  1. Chlamydia (Chlamydia trachomatis)
  2. Gonorrhoea (Neisseria gonorrhoea)
  3. Syphilis (Treponema pallidum)
  4. Genital mycoplasmas (Mycoplasma genitalium)
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6
Q

What is the “other” cause of STI?

A

Trichomoniasis (Trichomonas vaginalis)

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7
Q

What are the 2 pathologies that aren’t sexually transmitted infections by strict definition?

A
  1. UTIs - sexual contact can increase likelihood of exposure but doesn’t have to
  2. Candidiasis (“thrush”) - overgrowth of Candida albicans due to changes in vaginal flora - not transmitted
  3. Bacterial vaginosis - overgrowth of vaginal flora - not transmitted per se
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8
Q

1- Why has gonorrhoea advanced to 2nd place from 4th place in big 5?

2- Why are we seeing a decrease in HPV infections?

3- Why Is syphylis so detrimental? What is offered to all patients as a result of this?

4- What age group does Chlamydia affect most

A

1- Resistance to antibiotics

2- Standard vaccination programme against HPV. Vaccination with GardasilTM covers two high-risk strains (16 & 18) for cervical (and other) cancer, but also the two most prevalent low-risk strains for anogenital warts (6 & 11).

3- Often missed as primary symptoms disappear in their own. Late syphilis infections are associated with severe CNS complications and death.
> Syphilis serology should be offered to all patients

4- 15-25 years of age

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9
Q

What STI commonly recur?

A
  • Anogenital warts (HPV) and Genital herpes (HSV) show almost 50% recurrence
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10
Q

A significant, proportion of undiagnosed or treatment- refractory chlamydial infections go on to produce what disorder?

A
  • Pelvic-inflammatory disorder
    > Extremely serious and a potential complication of many of STI if left untreated
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11
Q

Why are HIV cases decreasing?

A
  • Ability of us to identify cases and provide antiretroviral treatments.
    > If you can reduce a patient’s viral load to “undetectable” then the infection cannot be transmitted by that person.

A patient with an UNDETECTABLE viral load cannot transmit HIV at all!
-All your patients who come for an STI screen should be offered testing for HIV

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12
Q

What are the 2 types of patients when it comes to STI?

A
  • Symptomatic : symptoms guid you
    > May need treatments there and then
  • Asymptomatic : patients may not have symptoms
    > Asymptomatic patients will need a little more questioning to discern what they might be at risk of.
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13
Q

What questions would you ask patients to learn about their last sexual contact?
How do you ask about their past sexual history?

A
  • You want to know if that site needs testing

*Past sexual history:
3 months is usually long enough. Ask all the same questions for each patient as for LSC

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14
Q

What other areas would you need to investigate in sexual health history?

A

1- Patient’s medical history:
Include asking about previous STI diagnoses! Remember recurrence is a problem

2- Drug and alcohol use:
Includes chemsex. Also, smoking…

3- Blood-borne virus (BBV) risk:
Not just HIV – includes hepatitis as well.. if they have a hepatitis risk - how would you manage this whilst you wait for results

4- Assess pregnancy
It might affect what drugs a patient can take if you do decide to treat them.

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15
Q

Women may need other questions asked such as…?

A

1- Last menstrual period:
2- Preferred contraception:
3- Pregnant women:
> Many (including the main ones) of the STIs can be passed from mother-to-child
> This can lead to trachoma, ophthalmia neonatorum and neonatal meningitis
4- Breastfeeding:
Affect certain drugs due to risk of excretion in breast milk

*This is also an opportunity to look out for anything else:
Abuse, FGM, etc.

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16
Q

What follows questioning?

A
  • Examination and sampling will follow, depending on the information you get!
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17
Q

Anogenital herpes is caused by what?

A
  • Human herpesviruses (HSV1 and HSV2) ; same as coldsores
    > Involves infection with virus or reactivation of pre-existing infection
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18
Q

What HSV group do HSV1/2 belong to?

A
  • Alphaherpesvirinae (dsDNA and enveloped)
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19
Q

How does Anogenital herpes spread?

A
  • Spread from person-to-person through secretions – HSV can infect any stratified squamous epithelium

> Extremely painful

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20
Q

1- What HSV is the most common cause of herpes in the UK?

2- What HSV is more likely to cause recurrence?

3- How often do recurrent herpes episodes occur?

4- What fraction of patients develop symptoms?

A

1- HSV-1

2- HSV-2

3- 4 episodes

4- 1/3

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21
Q

Name the 3 outcomes of infection from human herpesviruses (HSV1 and HSV2).

A
  1. Symptomatic infection (~33%) resulting in the classic vesicular, painful rash
  2. Latency in dorsal root ganglia… can lead to reactivation… which in itself can lead to…
  3. Viral encephalitis – talked about in Pathogens IV
22
Q

Human herpesvirus has primary,secondary and recurrent infection. Explain this.

A
  • Primary – No pre-existing Ig to virus
  • Secondary – Pre-existing Ig to virus present
  • Recurrent – Reactivation of latent infection
23
Q

How do doctor manage Anogenital herpes? What is the dilemma we have with managing herpes?

A
  • Acyclovir
  • Analgesia and reducing spread are key
    > Does not stop recurrence
    > The patient has prior T-helper cells and antibodies against the virus, but that does not stop them experiencing discomfort, embarrassment and risk of serious complications… nor does it stop them spreading it.
24
Q

What are the symptoms of primary Anogenital herpes infection?

A
  • Painful, irritated papules arise on penis/vagina/vulva/anus or other mucosal tissues
    > Usually ulcerative, vesicular and exudative
25
Q

Describe the immune response to Anogenital herpes.

A
  • Ongoing cell death and TH1 response lead to vesicles and ulcers with possible systemic symptoms of fever and myalgia
  • Symptoms abate at ~10 days
  • Generation of anti-virus CD8+ cytotoxic T-cells and neutralising Ig is responsible and results in memory

*Symptoms are often less severe in patients with secondary infection!
Papules and vesicles may be subclinical and identified only by specialist (or even non-visible)

26
Q

How do we detect Anogenital herpes?

A
  • Samples from vesicular exudate at affected sites sent for nucleic-acid amplification tests (NAAT) to confirm virus
  • Virus serotyping by immune methods needed
27
Q

What causes Anogenital warts?
- Name the Family
- Name the Genus
- Name the genome
- Name the 2 groups the virus are split into/ what different symptoms do they cause?

A
  • Human papillomavirus (HPV)= more than 120 types of papillomavirus
    > Family: Papillomaviridae
    > Genus: Papillomavirus
    > Genome: dsDNA = (non-enveloped)
28
Q

what are some cancers that can be caused by high risk HPV strains?

A

99% cervical cancers,
80-90% anal cancers,
36% oropharyngeal cancers,
50% penile cancers

29
Q

What do high risk/ low risk HPV do upon infection?

A
  1. Initial exposure to stratum basale cells
  2. Lysogenic replication - both alter the way the infected cell enters and leaves the cell cycle:

> LOW RISK STRAINS: cause symptoms or no symptoms which may undergo lytic replication and spread → cell-mediated and humoral clearance

> HIGH RISK STRAINS: cause irreversible replication with failures of error-checking → tumour formation

30
Q

What are the symptoms of primary anogenital warts infection?
Warts can be asymptomatic what are the clinical implications to be aware of tho?

A
  • Presence of warts on any squamous epithelium.
    > Classical features based on induced hyper-proliferation of stratum basale cells
  • Can be asymptomatic but still associated with transmission
31
Q

what are the 2 phases the immune system has for clearing the HPV infections (Anogenital warts) ?

A
  • Th1 response will cause regression when cytotoxic T-cells begin to kill off the infected stratum basale cells that are infected
  • Seroconversion when antiviral IgG is produced to prevent any reinfection of cells.
32
Q

1- How are HPV infections detected?
2- How do we manage HPV infections?
3- What are the Complications of HPV infections?

A

1- Most are “classical” and diagnosed by presentation

2- Multiple management attempts needed especially in recurrent infections
- drugs (podophyllotoxin, imiquimod)
- physical ablation (cryotherapy or excision) can be used but problematic/unpleasant

3-
- Recurrence is very common
- Infection with high-risk strains does not produce symptoms, but can be a massive risk for precancerous change

33
Q

What are the 4 minimum infections to be tested for on a standard STI screen.

A

-Chlamydia
-Gonorrhoea
With serology for:
-Syphilis
-HIV

34
Q

What bacteria causes Chlamydia?
What are the characteristics of this bacteria?

A

Chlamydia trachomatis
- No true cell wall in Chlamydiae – dual membrane and capsular serotypes

35
Q

What are the 2 forms of the Chlamydia bacterium?

A
36
Q

Describe the infective cycle of Chlamydia bacterium?

A
37
Q

1- What serotypes of Chlamydia trachomatis cause LGV (lymphogranuloma venereum)

2- What stereotype lead to urogenital infection/transient conjunctivitis?

3- What stereotype cause ophthalmic infection?

4- What serogroup cause trachoma?

A

1- L1/L2/L3

2- D-K

3- All

4- A-C

38
Q

What are the primary symptoms of Chlamydia trachomatis?
> What gender present as asymptomatic mostly?

A

Non-gonococcal urethritis (NGU)
*Variety of symptoms depending on location

  • Urethritis is most common presentation, but anal, pharyngeal and conjunctival infections possible
  • Dysuria, discharge and pain are common.
    Women may have cervicitis, dyspareunia, IM/PC bleeding as well
  • Eye infections = Trachoma (leading cause of reversible blindness worldwide)

> Men

39
Q

How is Chlamydia detected?

A
  • Swab of symptomatic area or first-catch urine
  • NAATs for detection
  • Culture needed for antimicrobial sensitivity
40
Q

What are the complications of Chlamydia?

A
  • Asymptomatic infections may persist for a year
  • Spread from primary site is a leading cause of pelvic inflammatory disease, epididymitis, orchitis and edometritis
  • Lead to infertility
  • Can lead to SARA (sexually-acquired reactive arthritis)
41
Q

Is chlamydia transmissible to new-born?

A
  • Yes (often leading to ophthalmia neonatorum).
42
Q

1- What bacteria causes Gonorrhoea?
2- What are the characteristics of this bacteria?

A

1- Neisseria gonorrhoea = Gonococcal urethritis
2-
- classic appearance as pairs of bean-shaped cocci
- belongs to same genus as N. meningitidis
- does NOT produce a capsule - thus no possibility of antibodies against it

43
Q

1- Where does primary infection of Gonorrhoea occur?
2- What are the primary symptoms of Gonorrhoea?

A

1- Columnar mucosal epithelium (urethra, rectum, pharynx and conjunctiva)

2- As with chlamydia, location of infection is important as symptoms may be different
- Male patients (~90%) will show symptoms of gonococcal urethritis
- Female patients (~50%) will show symptoms of cervicitis (urethritis rarer than men)
> Other sites often asymptomatic but discharge and pain are most common symptoms

44
Q

What gender does Gonorrhoea mostly present?

A
  • Males and mimic those of NGU.
    > Infections in other sites are likely following exposure and should be tested for based on the history results.
45
Q

How is Gonorrhoea detected in Asymptomatic and Symptomatic patients?

A
  • Asymptomatic urethral infection should be investigated by:
    > first-catch urine (in males)
    > self- taken vulvo-vaginal swabs (in females)
    and these should be subjected to nucleic-acid amplification tests (NAATs) for chlamydia and gonorrhoea.
    > Microscopy is of limited use if there is no discharge (as the pathogen number will be sparse) but culture for ID and antibiotic sensitivities will be of use.
  • Symptomatic
    > Discharge from any site should be sampled by swab and should be investigated through microscopy as this may show N. gonorrhoea and allows for diagnosis in less than 1hr.
    > Culture of swabs is essential for antibiotic sensitivities
46
Q

What are the complications of Gonorrhoea?

A
  • Uncontrolled infection will lead to deeper spread (PID and other damage to reproductive system)
  • Disseminated gonococcal infection through the blood can lead to serious problems in skin, joints, tendons
  • Long-term colonisation of deeper tissues can also be an issue, with infection flaring up again in places such as tendon sheaths.
  • Persistence at subclinical levels in genital and extragenital sites can be long-lasting (cannot become immune to gonorrhoea)
  • Babies may contract ophthalmia neonatorum during birth
47
Q

1- What is NGU now known to be caused by? What are the implications of this discovery?

A

1- NGU is now known to be caused by Mycoplasma genitalium, which shows a ~40% insensitivity to macrolides
> Likely responsible for many treatment failures
> Macrolide resistance in Chlamydia is increasing
> Treatment regimens updated!

If M. genitalium detected:
100mg oral doxycycline twice-daily for 7 days, followed by
azithromycin 1g orally (stat), followed by 500mg per day for two days
Moxifloxacin, oral 400mg once-daily for 10 days (where sensitivities known)

48
Q

What are the treatments for Chlamydia? ( Uncomplicated NGU)
Name the alternatives we can give too.

A
  • 100mg oral doxycycline twice-daily for 7 days

Alternatives:
> Azithromycin 1g orally followed by 500mg per day for two days (should be considered sub-optimal)
> Ofloxacin (oral 400mg once-daily for 7 days)

49
Q

What are the treatments for Gonorrhoea? (Uncomplicated gonococcal urethritis)

What alternatives can be given?

A

1g intramuscular ceftriaxone stat

  • Alternatives:
    > Gentamicin (240mg intramuscular injection stat)PLUS 2g oral azithromycin stat

> Cefixime (400mg oral stat) – if patient refuses injectionPLUS 2g oral azithromycin stat

> Ciprofloxacin (500mg oral stat) – if cephalosporins contraindicated AND sensitivities known

50
Q

What complicates Gonorrhoea and Chlamydia treatments?

A
  • Pregnancy and breastfeeding
51
Q

What MUST happen after treatment?

A
  • Test of cure recommended for all patients!
  • Treatment failures MUST be reported
52
Q

What is the problem we have Neisseria gonorrhoea?

A
  • One of the most dangerous antimicrobial resistance threats we have ever encountered. Since 1947 it has become resistant to benzylpenicillin, azithromycin, ciprofloxacin and now shows decreased sensitivity to ceftriaxone.

Unit 8 (15 decks)

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