Sexually Transmitted Infections

DR EDDY CHEAH
Session Jan 2018
 List of STIs

BACTERIAL INFECTIONS

Syphilis, gonorrhoea, chlamydial infections, PID, chancroid

VIRAL INFECTIONS

HIV/AIDS, hepatitis B, genital herpes, genital warts

PARASITIC INFECTIONS

Trichomoniasis, pediculosis pubis

 Syphilis

• CAUSATIVE AGENT – Treponema pallidum

• MODES OF TRANSMISSION
DIRECT, CLOSE CONTACT

 Enter a sexual contact via mucous membranes or minute skin

abrasions

 Sensitive to drying, heat, and disinfectants

TRANSPLACENTAL

 Higher risk after 1st trimester

 SYPHILIS

Lab Diagnosis

• MICROSCOPY
 Exudates from primary & secondary lesions

 Fluorescence microscopy with fluorescein-labelled anti-treponemal

antibodies

• SEROLOGICAL TESTS
 VDRL & RPR tests  detect an antibody-like substance called
reagin

 Treponema pallidum particle agglutination test (TPPA)

 SYPHILIS

Treatment

• INITIAL INFECTION
 Single intramuscular injection of benzathine penicillin

• OLDER INFECTION
 3 intramuscular injections of benzathine penicillin at weekly
intervals

• Ceftriaxone if allergic to penicillin

 Gonorrhoea

HOST EVASION

• Antigenic variation – pili proteins, OM proteins

• Pili and OM proteins interfere with phagocytosis
• Catalase production & antioxidant defence system
• IgA protease inactivates IgA in mucous secretions
• Intracellular multiplication protects from phagocytes and
antibodies
 Gonorrhoea

CLINICAL FEATURES

• MEN → mostly symptomatic

* Urethritis – purulent urethral discharge, dysuria

• WOMEN → mostly asymptomatic

* Cervicitis – cervico-vaginal discharge, cervical oedema,
abnormal menses, dyspareunia, dysuria, abdominal pain

* Untreated, asymptomatic women → pelvic inflammatory

disease (PID)
 Gonorrhoea

LAB DIAGNOSIS

• Swabs – urethral, cervical, rectal, pharyngeal

• Microscopy → Gram-negative diplococci, kidney bean-shaped
• Culture on Martin-Lewis agar
* Enriched selective chocolate agar

* Antibiotics: Vancomycin (Gram positives), colistin & trimethoprim

(Gram negatives), anisomycin (fungi)

* Culture ID via API/VITEK test

• PCR → usually in combination with Chlamydia detection

N. gonorrhoeae colonies on Martin-Lewis agar

Source: Hardy Diagnostics

 Gonorrhoea

TREATMENT

• Ceftriaxone → intramuscular injection

• Cefixime → oral administration
• Co-infection with Chlamydia trachomatis → +
azithromycin/doxycycline

• Gonococcal Antimicrobial Surveillance Programme (WHO) →

resistance to penicillin, quinolones, and azithromycin
 Life cycle forms of chlamydiae

ELEMENTARY BODY RETICULATE BODY

• Smaller in size
• Rigid cell wall
• Metabolically inert
• Infectious form
• Adapted for extracellular
survival
• Larger in size
• Fragile cell wall
• Metabolically active
• Non-infectious form
• Adapted for intracellular
growth
 Chlamydial Infections

LAB DIAGNOSIS

• Cell culture:
* Genital infections → urethral/cervical swabs

* LGV → bubo pus/tissue biopsy

* Detection via fluorescein-labelled antibodies

• PCR tests → urine, urethral/cervical swabs, tampons

• Chlamydia screening programmes
 Genital Warts

• PATHOGENESIS & CLINICAL FEATURES

* Specifically attacks skin & mucous membranes → squamous
epithelial cells

* Virus replicates slowly → stimulates uncontrolled division of

host cells → clusters of pinkish-brown-masses, WARTS, on
the genital

* Warts usually found on vaginal opening or perianal

* However, most infections are subclinical

 Genital Warts

• ONCOGENESIS
* Viral genome is not integrated into host cell’s genome →
benign human lesions

* Part of the viral genome integrated into host cell’s genome →

malignant tumour

* Viral transforming genes → E6 and E7

* E6 degrades p53 (tumour suppressor) while E7 interacts with

pRB to abrogate cell cycle regulation
 Genital Warts

• DIAGNOSIS
* Clinical and histological examination

* Pap smear → detects the presence of abnormal cells (nuclear

enlargement & perinuclear cytoplasmic vacuolisation)

* PCR test

• TREATMENT
* Topical cytotoxins → e.g. podophyllotoxin, 5-FU, TCA

* Cryotherapy, laser therapy, surgical excision

Stages of cervical cancer carcinogenesis

Source: CDC
 Genital Warts

• VACCINATION
* Mainly for women to protect against the HPV types that
cause cervical cancer

* Microbial subunit vaccines → L1 polypeptide expressed in

yeast

* Bivalent → protection against HPV types 16 and 18

* Quadrivalent (Gardasil) → protection against HPV types 6,

11, 16 and 18
 Gonorrhoea

• LAB DIAGNOSIS
 PCR tests & serological tests

• TREATMENT
 Aciclovir / valaciclovir / famciclovir

 Does not eliminate latent infection!

• TREATMENT
 Total abstinence from sex

 Caesarian delivery for symptomatic pregnant women

 HIV/AIDS

• CAUSATIVE AGENTS – HIV-1, HIV-2

• INCIDENCE
* 36.7 million cases at the end of 2016

* Highly prevalent in Africa and developing countries of Asia

• MODES OF TRANSMISSION
* Through unprotected sexual intercourse

* Through blood → transfusion, sharing of needles

* Mother to child → during pregnancy/childbirth, breast feeding

 HIV/AIDS

TREATMENT

• Nucleoside RT inhibitors – e.g. zidovudine

• Non-nucleoside RT inhibitors – e.g. efavirenz
• Protease inhibitors – e.g. ritonavir
• Integrase inhibitors – e.g. elvitegravir
• Antiretroviral therapy (ART) → combined drug therapy for
effective treatment

• Side effects & high daily pill burden → non-compliance

 HIV/AIDS

Why is it challenging to develop an effective vaccine?

• High mutation rate of HIV

• Presence of HIV-1 and HIV-2 strains

• Narrow window of opportunity to clear initial infection

• Ethical issues in testing of candidate vaccines

 Trichomoniasis

• CAUSATIVE AGENTS – Trichomonas vaginalis

• SITES OF INFECTION – vagina (F), urethra (M)
• Oval-shaped, multiple flagella
• Lacks a cyst form
• Vaginitis → vaginal discharge & itching, dyspareunia, dysuria
• Co-infection with gonorrhoea → risk of PID
• Pregnancy → premature babies with low birth weight