Types Non sexually transmitted Sexually acquired

Infections of Bacterial vaginosis/ Candidiasis Chlamydia Gonorrhoea Genital warts Genital herpes Syphilis Trichomoniasis
vulva & vagina Gardnerella/ (thrush) (condylomata
(V/V) anaerobic vaginosis acuminata)
Definition Overgrowth of Overgrowth of STI caused by gram STI caused by gram Infection of V/V or Genital infection STI caused by the Genital infection
predominantly naturally occurring negative, Chlamydia negative diplococcus, cervix with the caused by herpes bacterium caused by protozoa
anaerobic organisms Candida albicans trachomatis Neisseria gonorrhoeae human papilloma simplex virus (HSV) Treponema pallidum Trichomonas vaginalis
virus
Epidemiology Found in 12-30% of  Most common  Most common STI  2nd most common  Very common  Common  Uncommon but  Common worldwide
women cause of vaginal  5-10% of women bacterial cause STI in  50% of sexually  US - 45 million increasing but relatively rare in
infection aged 20-30 have the UK with active adults have infected, with new  2680 cases in the UK UK
 Found in 20% of been infected prevalence of 22,000 genital HPV infections 1 in 2007  Prevalence 2-3%
women, often cases million/year
asymptomatic  Largely HSV-2, but
genital HSV-1
infections are ↑
Aetiology  Anaerobic organism  Alkaline vaginal pH  Trasnmitted by  Transmitted by sexual  Transmitted by  Sexual contact  Sexual contact  Sexual contact
replaced normal  Change in sexual contact (30- contact (75%) physical or sexual  Direct contact (lesion  Blood borne
lactobacilli protective bacterial 40%)  Vertical (neonatal contact or body fluid)  Vertical (congenital
 Increase in vaginal pH flora  Vertical (50%) conjunctivitis)  Occasionally vertical  Vertical syphilis)
Risk factors  Smoking  Pregnancy  Multiple sexual  Multiple sexual  Multiple sexual  Unprotected sex  Unprotected sex  Multiple sexual
 IUS/IUCD  Diabetes partners partners partner  Multiple partner  Multiple partner contact
 Vaginal douching  Antibiotics,  Age <25 years  Age <25 years  Unprotected sex  Hx of STI  HIV  Unprotected sex
immunosuppression  Hx of STI  Presence of other STI  Immuno suppression  1st intercourse at  Presence of other STI
 Vaginal douching  Low SE status  Smoking early age
 Sexual activity (little  Low SE status
evidence)  Immune
compromised
History  Offensive ‘fishy’  Vulva irritation and  Usually  50% asymptomatic  Often asymptomatic Primary: Primary:  Offensive grey-
odour (amines itchiness asymptomatic 75%)  PV discharge  Wart on V/V, cervix  Multiple inflamed  Solitary painless green/yellow
released by bacterial  ‘cottage cheese-  Pv discharge  IMB, PCB and anus painful vesicles, vulval ulcer discharge (sometime
proteolysis) grey- like’ discharge  Urethritis  Dysuria  Painless but may papules and ulcers (chancre) frothy)
white discharge  Superficial  Dyspareunia  Dyspareunia itch, blled and around the introitus,  Infectious  V/V irritation
 Vagina is not red or dyspareunia and  IMB, PCB  Urethritis inflamed resembling cold sores  Develop after 10-90d  Dyspareunia
itchy dysuria  Abdominal pain  Bartholinitis  Dysuria incubation  Dysuria
 50% asymptomatic  Dysuria  Cervivitis  Cervicitis  Disappear  Maybe
 PV discharge spontaneosly after 1 asymptomatic
Examination  Grey-white PV Speculum – V/V red  Lower abdominal  Mucopurulent  Pink/ red/ brown  Systemis symptoms – week  Diffuse/patchy
discharge & inflamed. White tenderness endocervical discharge papules (single or fever, headache Secondary: punctate
 Rarely - secondary  Maculopapular rash,
  Characteristic smell plaque may be  Vaginal tenderness/  Easily induced multiple) bacterial infection, influenza like eryhthematous
observe on the V/V excitation endocervical bleeding  4 common aseptic meningitis, symptoms and warty cervical lesion
wall  Speculum: cervicitis, appearances: small acute urinary genital or perioral (strawberry cervix)
cervical/ urethral papules, retention growth
discharge ‘cauliflower’,  Local (condylomata lata),
keratotic and flat lymphadenopathy arthralgia
papules/plaque. Reactivation:  1-10 weeks after
 Occur in 75% appearance of
 Less painful, less chancre
severe Tertiary/Latent:
 Often preceded by  1-20 years after
localized tingling initial infection
 Neurosyphilis
(paresis, dementia,
psychosis, epilepsy,
tabes dorsalis)
 Cardiovascular
syphilis (aortitis, AR,
HF, angina)
 Gummatous syphilis
(granulomatous
lesion in skin, bone)
Pathophysiology  Poorly understood  Yeast infect  Chlamydia consists  Affects mucous  Infect epithelial cells  In latency, sacral  Survive only briefly  Flagellated protozoa
 Often involved epithelial cells of an infectious membrane, causing them to nerve root ganglia outside the body infests vaginal
organisms –  Develops spores & elementary body transmitted by multiply abnormally (S2-S5) are involved  Require direct epithelium
gardnerella vaginalis, pseudohyphae and an intracellular inoculation of infected  >100 subtypes are  Humans are the only contact for  Proliferate when pH
mycoplasma hominis, reticular body secretion from one known reservoir transmission >5
prevotella sp.  Elementary body mucosal surface to  Low risk type (6&11)  Inactivated at room  Invades abraded skin
attaches to and is another – bening genital temperature and by or mucous
taken up by wart drying membrane and
epithelial cells  High risk type  Asymptomatic virus disseminates rapidly
 Intracellular (16&18) – CIN & VIN shedding is thought via blood or
reticular body to be the most lymphatic system
replicates by binary common HSV-2
fission transmission
 Cells bursts
releasing more
infectious
elementary bodies
Investigations Amsel’s criteria(3/4):  HVS  culture  Nucleic acid  Endocervical swab/  Often clinical dx  HVS  culture  Rapid Plasma Reagin  Wet film microscopy
  Typical white  Rec. Inf: screen for amplification test HVS  culture  Biopsy of lesion  PCR & DFA (RPR), syphilis (shows presence of
homogenous diabetes (NAAT) e.g. PCR  Cervical smear enzyme flagellated protozoa)
discharge  Perform on immunoassay (EIA),  HVS  culture
 Raised vaginal pH endocervical swab, Venereal Disease
 Positive ‘whiff’ test HVS or 1st void urine Research Laboratory
(fishy odour when samples (VDRL)
10% KOH added)  Can give false
 ‘Clue cell’ (epithelial positive with EBV,
cell with attached TB, lymphoma,
bacterial) on malaria
microscopy  Combine with
Treponema pallidum
haemagglutination
(TPHA) and
Fluorescent
Treponemal
Antibody –
Absorption (FTA-Abs)
Management  PO metronidazole or  Cotton underwear  Doxycline 100mg bd  Cephalosporin,  Imiquimod cream or  No drug can cure  Penicillin G (all  Metronidazole
topical clindamycin & avoid douching x1/52 or single dose penicillin (in UK, podophyllin (both CI  Aciclovir, valaciclovir stages), usually IM or  Require full STI
 Avoid vaginal  Topical clotrimazole of azithromycin 1g ciprofloxacin and in pregnancy) or famciclovir is used  Oral tetracycline or screening and
douching e.g. Canestren or  Pregnancy: penicillin resistance  Cryotherapy, laser or in severe infection  doxycycline (CI in contact tracing
oral flucanozole (CI erythromycin/ ↑), ceftriaxone electrocautery (used make symptoms less pregnancy)
in pregnancy) amoxicillin required. for resistant) severe  Follow up clinically
 Treat partner if  Full STI screening  Tetracycline or  HPV vaccine (aim at  ↓duration of and serologically at
recurrent thrush and contact tracing quinolone (single subtypes 6, 11, 16. symptoms if started 1, 2, 3, 6 and 12
dose) 18) early in a reactivation months then 6
 Full STI screening and monthly until
contact tracing seronegative
 Require full STI
screen and contact
tracing
Complications  2o infection in PID Disruption to social  PID  PID  Cervical cancer  Herpes meningitis  Cardiovascular  Strongly associated
 ↑ risk of endometritis and sexual life  Chronic pelvic pain  Chronic pelvic pain  Vertical: laryngeal  Herpes encephalitis disease with the presence of
following TOP  Tubal damage   Infertility papillomatosis  Eczema herpeticum  CNS disease other STI
 ↑risk of vaginal cuff subfertility  Conjunctivitis  Herpetic whitlow  Jarisch Herxheimer  PID
cellulitis after vaginal  Reiter’s syndrome  Fitz-Hugsh-Curtis  Ocular herpes and reaction (febrile  Infertility
hysterectomy (arthritis, urethritis, syndrome vision loss reaction to tx, with  ↑ transmission HIV
 Associated with conjuctivitis) (perihepatitis)  Pregnancy: fever, chills, myalgia)  Pregnancy: PTL,
miscarriage, PTL,  Fitz-Hugh-Curtis  Systemic: arthralgia, miscarriage, PRL,  Congenital syphilis PPROM
 PPROM acute monoarticular IUGR,  ↑susceptibility to
syndrome septic atrhitis,  Vertical (rare): HIV
(perihepatitis) meningitis, neonatal herpes
 Pregnancy: PTL, endocarditis) (meningitis,
PPROM, post  Vertical: opthalmia encephalitis, mental
partum neonatorum (bilateral retardation)
endometritis conjunctivitis)
 Vertical: neontal
conjunctivitis (35-
50%), neonatal
pneumonia (10-
20%)

Prognosis 50% recurrence  Good with tx  Good with tx Cure rate is 95% with tx  HPV causes 3-4% of  Outbreak symptoms Excellent with tx in Cure rate is 90% with
 Recurrent in 5% - (problem is most genital cancers become less severe primary or secondary antibiotics
common in immune case are  HPV 16&18 causes with time as syphilis
compromised asymptomatic) 70% of cervical antibodies develop
 Long term infection cancer  Until no longer
associates with outbreaks, though
infertility they may still be
contagious to others
 Neonatal herpes has
a high mortality but
can be prevented by
acyclovir

Principle in management of STI

 Screening for concurrent STI

 Screen and treat regular sexual partner
 Contact tracing – recent sexual partner – screen and treat
 Manitain confidentiality
 Education – changing partners ↑ risk of STI, STI can occur in monogamaous relationship e.g. genital herpes following orogenital sex
 Barrier method – contraception ↓ risk of STI