Sexually transmitted infections Flashcards

1
Q

Basic rules for clinical practice with managing STIs

A
  • Reassure and treat with kindness
  • Remove all shame and stigma
  • Open door policy
  • test and treat at presentation
  • consider culture before treatment
  • exclude pregnancy
  • offer OCP, Coil, HBV vaccine
  • Test and treat all partners
  • No SI for 7 days after both have been treated
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2
Q

Sequalae of STIs

A
  • Morbidity and mortality from sepsis
  • chronic pain
  • infertility
  • vertical transmission - congenital and neonatal infection
  • altered HIV transmission
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3
Q

What factors affect how infectious an STI is (4)

A
  • probability of transmission in a contact
  • frequency of contacts in the populations
  • Duration of infectiousness
  • proportion of the population that is already immune
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4
Q

What is the basic reproductive rate (R0)

A

The average number of individuals directly infected by an infectious case (secondary cases) during his or her entire infectious period when he or she enters a totally susceptible population
R<1 the disease will disappear
R=0 it will become endemic
R>1 there will be an epidemic

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5
Q

The actual value for R0 can be calculated

What are the factors

A

B - risk of transmission per contact (attach rate) - condoms, face masks, hand washing help with this
K - average contacts per time unit - isolation
D- duration of infectiousness - same time unit as K
Disease specific
R0 = B x K x D

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6
Q
Chlamydia trachomatis 
What is it 
Epidemiology
Pathophys 
risk factors
A

Obligate intracellular parasite - Three human biovars
Ab, B, Ba, C - eye infection
D-K - PID / urethritis
L1,2,3 - lymphogranuloma venereum

Most common - 70% infections in under 25 year olds
High frequency of transmission partner concordance 75%
15-24 yo 5 % 30% in homeless youth
Risk factors:
More then one sexual partner in 12 months
Recent change in partner, concurrent partners
Inconsistent condom use
Drugs, alcohol, substance use

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7
Q

Chlamydia trachomatis
Symptoms
Complications

A

70% asymptomatic
Mucopurulent cervical discharge , Dysuria, Dysparunia
Pelvic pain, Abnormal bleeding, Conjunctivitis
Rectal and pharyngeal infections are usually asymptomatic
Perihepatitis - FHC
Cervicitis - contact bleeding - IMB, PCB

PID <1% - up to 30%
Increased risk if infections recurrent
Reinfection 10-30%
Prolonged infection (persistent or reinfection) major risk for tubal damage
Associated with ectopics and infertility
Neonatal infection
Reactive arthiritis
Perihepatitis 

Pregnancy

  • PPROM
  • PTB
  • LBW
  • 60-70% exposed infants acquire infection - neonatal conjunctivitis and pneumonia
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8
Q

Chlamydia

Testing and tx

A

Test when presents and 2 weeks later as if sexual exposure within 2 weeks then test will not be positive
NAAT Nucleic acid amplification test
Vaginal or cervical swab, first catch urine, pharyngeal, rectal, conjunctiva
Self swabs are no less effective then clinician taken swabs
Firs tpass urine not as good as self swabs

1G stat Azithromycin
Doxy 100mg BD for 7 days - contraindicated in pregnancy, 1st line in rectal infections
In pregnancy test of cure in 4-6 weeks
Rescreen 3/12
Emerging evidence of some resistance to azithromycin up to 5%
Treat if high index of suspicion
Start partner treatment without waiting for lab results
Other immediate management
• Advise no sexual contact for 7 days after treatment is administered.
Contact tracing for the last 6 months

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9
Q
Neisseria gonorrhoeae
What is it 
Epidemiology
risk factors 
Complications
A

Gram stain negative intracellular diplococcus
Men present more with sx, risks are MSM, indigenous populations, high risk areas, travellers
Often asymptomatic 80% in woman
Discharge, dysparunia, cervicitis, anorectal symptoms, conjunctivitis
Can disseminate in immunosuppressed, pregnancy - septic joints, macular rash with necrotic pustules, rarely meningitis or endocarditis
pharyngeal carriage
Co infection with Chlamydia is common
PID

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10
Q

Gonorrhoea testing and tx

A

Test at first presentation and repeat after 2 weeks in sexual exposure within previous 2 weeks
NAAT on vaginal or cervical swabs, first catch urine, pharyngel, rectal, conjunctival, joint aspirates
If local symptoms then do a culture on vaginal swabs
Gram stain to visualise for diagnosis
Culture must be done, to exclude resistance
Ceftriaxone 500mg IMI stat with 1% lignocaine + Azithromycin (always co treat) 1 g po STAT
Test of cure 2 weeks later
Rescreen 3/12
 Advise no sexual contact for 7 days after treatment is administered.
 Advise no sex with partners from the last 2 months until the partners have been tested and treated if necessary.
 Contact tracing

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11
Q
Mycoplasma Genitalium
What is it 
Epidemiology
risk factors 
Complications
Test
A

Bacteria
Often asymptomatic
Discharge and dysuria, PCB, IMB, pain
Unknown role in PID and infertility
Causes non gonnacoccal urethritis
Established cause of urethritis, cervicitis and PID, ectopic
preterm delivery and miscarriage
DO not need to screen asymptomatic people - just people with sx
NAAT on endocervical swab, vaginal swab or FPU (not as sensitive)

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12
Q

treatment mycoplasma

A

Can be difficult to treat
Doxycycline 100 mg BD 7/7 followed by azithromycin 1g stat then 500mg daily for 3/7
If it is macrolide resistance (AS in half of infections esp MSM) - doxy 100 mg BD 7/7 followed by moxifloxacin 400mg daily 14 days

If PID from mycoplasma genitalium then moxifloxacin 400mg daily 14
 Advise no condomless sex until tested for cure (14 days after completion of treatment).
 Advise no sex with untested previous sexual partners.
 Provide patient with factsheet
 M. genitalium is not a notifiable condition.
 Advice contact tracing although time window is unknown

TOC 4 weeks after commencing therapy

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13
Q

Treponema pallidum
What is it
risk of vertical transmission?
What are the risks to a pregnancy ?

A

T pallidum spirochete bacteria gram negative - Obligate parasite
• Congenital: (in utero or at delivery)
• 70% if primary or secondary
• 40% early latent
• 10% late latent
• Increases the risk of vertical transmission of HIV and other STIs

  • 50% of woman suffer adverse pregnancy outcomes
  • 25% second trimester miscarriage or stillbirth
  • 11% neonatal death at term
  • 13% PTB or LBW
  • Placental infiltration reduces blood flow to the fetus and leads to growth restriction
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14
Q

What are the stages of syph

A

Primary syph is 1-3 weeks after exposure to infection, syphilitic chancre (painless)
Hard base, raised borders, fluid rich in spirochetes, very infectious
Chancre can be around external genitialia but if through contact can occur anywhere
Chance will heal on its on over months - can have associated lymphadenopathy
(if through blood may not be ) 30% unnoticed
Dark microscopy, PCR positive, serology can be negative as early phase of infection
Secondary 6-12 weeks after infections - spirochetaemia - Generalised lymphadenopathy
Can affect endothelial cells - causing non itchy maculopapular rash - trunk then travels to palms, soles, Can be pustular or papulosquamous
Can be condyloma lata wart like (smooth white painless gentials, anal, armpits)
Secondary syph is most infectious - lasts weeks to months
Latent phase - Disease - dormant / asymptomatic - stored in organs
Early phase - within a year, spirochetes can reenter the blood - can have sx of secondary syph
Late phase - after 1 year - will stay within organs
Tertiary syph - Type 4 hypersensitive reaction, immune reaction with T cells, pro inflammatory phagocytes and cytokines TNF IL 1 IL 6 leading to Redness warmth systemic sx like fever
Antigen on T Pallidum : group specific antigen
Species specific antigen
Cardiolipid (within spirochetes and cells in our body)
Granulomatous lesions - Gumma - immune cells surrounded by fibroblasts - often no spirochetes in there, Can necrose
Teritiary syph - cardiovascular - endarteritis (inflammatory of the vessels)
Brain and spinal cord - loss posterior spinal cord - loss of proprioception or vibration
Or anterior cord - paralysis
Liver joints and testes
Congential: transplacental or transvaginal

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15
Q

What are the 2 options of approaches for population based screening for syph?

A

“Traditinal algorithm”
High prevalence - use non treponemal (VDRL) and confirm with treponemal specific test (TPPA)

If low prevalence setting use treponemal (TPPA) and confirm with non (VDRL) less work and better sensitivity
Pregnancy RPR - should be used / IgG based test (IgM increases false positive results)

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16
Q

What are the fetal consequences of syph

A

2/3 babies born without sx
Placental or at birth through contact with secretions
30% who survive 30 days will have sx of congential syph
Neurological and developmental delays
MSK problems

Early - IUD jaundice, Hepatosplenomegly, maculopapular rash, palms and soles, pneumonia, coombs negative HA snuffles Mucocutanous lesions of palms and soels peristitis

Later - hutchinsons teeth (notched central teeth) saddle nose, frontal bossing, saber shin deformity, knee synovitis
Hutchinsons triad - hutchinsons teeth, interstitual keratitis, deafness

17
Q

How to treat syph

A

Primary, secondary, early latent - Benzathine Penicillin G 1.8g - single treatment dose
NOT short acting penicillin
Late latent syph - 1.8g IM Penicillin G for 3 weeks
If penicillin allergic HIV neg primary secondary or early latent then can use doxy
If tertiary, pregnant, HIV +, should have penicillin desensitisation

Can have jarisch - herxheirmer syndrome - as spirochetes are treated then explore and a large inflammatory reaction is activated

18
Q

What is BV

A

A polymicrobial clinical syndrome caused by a profound change in vaginal microbiota from a Lactobacillius dominant state to one with high diversity and loads of anaerobic bacteria including Gardnerella vaginalis, Atopobium vaginae, Mobiluncus spp, Prevotella spp, and other BV-associated bacteria (BVAB). This change is accompanied by a rise in vaginal pH and increased amines which produce odour. Studies have identified a polymicrobial biofilm adherent to vaginal epithelial cells of women with BV which is absent in controls.

19
Q

BV symptoms and presentation

A

 Most common cause of abnormal vaginal discharge in women of childbearing age
 Up to 50% are asymptomatic
 While BV is not considered an STI BV can be acquired through sexual activity
Offensive fishy discharge
Thin white homogenous discharge
Mild vulval irritation

20
Q

BV and pregnancy risk / complications

A

Bacterial vaginosis is associated with increased risk of spontaneous abortion, premature labour, chorioamnionitis, postpartum endometritis and pelvic inflammatory disease (PID); especially following termination of pregnancy (TOP), intra-uterine device (IUD) insertion or other instrumentation). BV is associated with a 2-3 fold increased risk of acquiring STIs including chlamydia, gonorrhoea, herpes simplex type 2 and HIV infection, and increases the risk of HIV transmission to male partners.

21
Q

Tests for BV

A

The diagnosis of BV is usually made in clinical settings using the Amsels or modified Amsels criteria;
A diagnosis is made if 3 or 4 of the following criteria are present:
1. Thin white/grey homogenous discharge –
2. Vaginal fluid raised pH (pH>4.5) – using pH paper
3. Positive whiff-amine test (presence of a fishy odor when 10% KOH is added to a sample of vaginal discharge)
4. Clue cells on gram stain (epithelial cells covered in bacteria)

Other:
•	Gram stain
•	Diagnostic cards (rapid tests)
•	Culture (G.Vaginalis)
•	DNA probes (G.Vaginalis)
•	PCR based test (G.Vaginalis)
•	Pap smear (not diagnostic)
examination
22
Q

BV tx

A

Symptomatic or woman under going gynae procedure
Metronidazole 400mg BD 7/7
Clindamycin 300 mg BD 7 days
Can also give Metronidazole/ clindamycin vaginally

23
Q

What is the pretest discussion pre HIV testing involve

A

Pretest discussion before performing the test
• permission
• how and when to give results
• explain the windowm period
• Good and easy treatment
• People with HIV have a normal life, partners, children, study and work
• and if they have support at home if they were positive

24
Q

Waht is the life cycle of chlamydia ?

A

Small gram-negative bacterium, obligate intracellular bacterial parasite

Biphasic life cycle: two morphologically and functionally distinct forms:

  • The small elementary bodies attach and penetrate into cells, changing into the metabolically active form, called the reticulate body, within six to eight hours. These forms create large inclusions within cells.
  • The reticulate bodies then reorganize into small elementary bodies, and within two to three days the cell ruptures, releasing newly formed elementary bodies. Release of the elementary bodies initiates the replicative process, since this is the form which can infect new epithelial cells. The long growth cycle explains why prolonged courses of treatment are necessary.
25
Q

What is trichomonas?

A

The responsible organism is the flagellated protozoan trichomonas vaginalis, which may be found in the vagina, urethra, and paraurethral glands of infected women. Other sites include cervix, Bartholin’s and Skene’s glands. Although survival on fomites has been reported, trichomoniasis is virtually always sexually transmitted.

overall prevalence of T. vaginalis is thought to be approx 3%,

26
Q

Trich clinical presentation

A

Classic signs & symptoms include purulent, malodorous, thin discharge (70%) with associated burning, pruritus, dysuria, frequency, and dyspareunia. Postcoital bleeding can occur. Urethra is also infected in the majority of women. Symptoms may be worse during menstruation. Classically described green, frothy, foul-smelling discharge is found in <10% of symptomatic women
Physical examination often reveals erythema of the vulva & vaginal mucosa; the classic green-yellow frothy discharge is observed in 10 to 30% of affected women. Punctate hemorrhages may be visible on vagina & cervix (“strawberry cervix” = 2% of cases).

27
Q

Trichomonas complications

pregnant and not

A

Trichomoniasis is a risk factor for development of post-hysterectomy cellulitis, tubal infertility, and cervical neoplasia. Another concern is that the infection facilitates transmission of HIV.

Pregnant women — consequences of trichomoniasis are potentially important in pregnant women in whom infection is associated with PPROM & PTB; however, treatment of asymptomatic infection has not been shown to reduce these complications.

28
Q

What are the causes of vaginitis

A
Common 
Infections: 
BV 
Candidiasis
Trichomonas
Less common
Foreign body
Desquamative inflammatory 
GAS
Ulcerative vaginitis associated with staph aureas and TTS
Idiopathic vulvovaginal ulceration 
Non infectious:
Chemical irritant
Allergic
Traumatic
Atophic
postpueral atrophic
Erosive lichen planus 
idiopathic
collagen vascular disease, Behcets, pemphigus syndrome
29
Q

What is the physiological of normal vaginal secretions

A

normal vaginal discharge consists of 1 to 4 mL fluid (per 24 hours), which is white or transparent, thick, and mostly odorless. This physiologic discharge is formed by mucoid endocervical secretions in combination with sloughing epithelial cells, normal bacteria, and vaginal transudate.

The pH of the normal vaginal secretions is 4.0 to 4.5;
Under the influence of estrogen, the normal vaginal epithelium cornifies and produces glycogen, which acts as a substrate for lactobacilli, thereby protecting women against infection from a number of pathogens.

In premenarchal and postmenopausal women in whom estrogen levels are low, the vaginal epithelium is thin and the pH of the normal vaginal secretions is 4.7 or more. The higher pH is due to reduced colonization of lactobacilli

30
Q

BV complications

A
  • Pregnant women with BV are at higher risk of preterm delivery
  • Causal relationship between BV and endometrial bacterial colonization, plasma-cell endometritis, postpartum fever, post-hysterectomy vaginal cuff cellulitis, and postabortal infection
  • BV is a risk factor for HIV acquisition and transmission
  • BV is a risk factor for acquisition of HSV-2, gonorrhea, and chlamydial infection.
  • BV is more common among women with PID, but it is not clear if it is an independent risk factor
31
Q

BV pathophysiology

A

BV is not due to a single organism. Instead it represents a complex change in the vaginal flora characterized by a reduction in concentration of the normally dominant hydrogen-peroxide producing lactobacilli and an increase in concentration of other organisms, especially anaerobes. These include Gardnerella vaginalis & Mycoplasma hominis.