Common Bacteria, Fungi & Parasites Causing Sexually Transmitted Infections
Overview of Sexually Transmitted Infections (STIs)
>>More than 30 distinct bacteria, viruses & parasites transmitted via sexual activity
>>Daily, 1\text{ million} curable STIs acquired world-wide (age 15\text{–}49)
Eight pathogens account for greatest disease burden (WHO 2016)
Curable: Syphilis, Gonorrhoea, Chlamydia, Trichomoniasis
Incurable: Hepatitis B, Herpes, HIV, HPV
WHO 2022 estimates
8\text{ million} adults (15–49 y) acquired syphilis
1.1\text{ million} pregnant women infected → >390\,000 adverse births
Bacterial STIs
• Treponema pallidum (Syphilis)
• Neisseria gonorrhoeae (Gonorrhoea)
• Chlamydia trachomatis (Chlamydia, LGV)
• Haemophilus ducreyi (Chancroid)
• Klebsiella granulomatis (Granuloma inguinale)
• Chlamydia trachomatis serovars L1-L3 (LGV)
• Gardnerella vaginalis (Bacterial vaginosis – linked to sexual activity)
Fungal Conditions Associated With Sex
• Tinea cruris (Jock itch) – Trichophyton rubrum, Epidermophyton floccosum
• Genital Candidiasis – Candida albicans (opportunistic; not strictly STI)
Parasitic Conditions
• Trichomoniasis – Trichomonas vaginalis
• Pediculosis pubis – Pthirus pubis
• Scabies – Sarcoptes scabiei (rarely sexual-only)
Core Laboratory Procedures
Dark-field microscopy → Syphilis spirochetes
Gram stain → Gonorrhoea, NGU, Chancroid, BV
Wet mount → Trichomonas vaginalis
10\% KOH mount → Candidiasis
Bubo aspiration/smear → LGV, Chancroid
NAATs, serology, culture per organism (details below)
Syphilis (Treponema pallidum ssp. pallidum)
Biology
Spirochaete: 6\text{–}15\,\mu m long, 0.25\,\mu m wide; microaerophile; fragile ex vivo
Few/no surface proteins; coats itself with host fibronectin → immune evasion
Transmission & Course
Sexual, trans-placental, transfusion, direct skin breach
Incubation 10\text{–}90 days (avg 21)
Untreated progression: Primary → Secondary → Latent (early, late) → Tertiary
Treat: single IM benzathine penicillin G (alt: doxycycline, macrolide, tetracycline)
Pathogenesis Highlights
“Great imitator”; highly invasive, low toxin production
Endoflagella give motility → endothelial adherence
Host reaction → endarteritis + plasma-cell infiltrate ⇢ tissue damage
Tertiary gumma = type-IV hypersensitivity (sensitized T-cells, macrophages)
Outer sheath lacks immunogens; TH1 down-regulated; antibodies vs cardiolipin, etc.
Clinical Phases
Primary – painless chancre; rich in organisms; heals 4–8 wk
Secondary – hematogenous spread → maculopapular rash (palms/soles), condylomata lata, fever, lymphadenopathy; most infectious
Latent – sero-positive w/o signs; early (<1 y) still infectious; late mainly non-infectious but vertical spread possible
Tertiary (yrs 1–30) – cardiovascular (aortitis), neuro-syphilis, gummas
Laboratory Diagnosis
Dark-field microscopy (motility); silver stain (Warthin-Starry, Steiner)
Serology
Nontreponemal: VDRL, RPR (titres; four-fold change significant)
Treponemal: FTA-ABS, TPHA/TPPA, AIA
Seroconversion ≈ 3\text{–}6 wk; follow-up VDRL at 1,3,6,12 mo post-therapy
Gonorrhoea (Neisseria gonorrhoeae)
Biology & Growth
Gram-negative, oxidase+ diplococcus; facultative anaerobe; intracellular in PMNs
Requires 5\% CO₂; cultured on Thayer–Martin VPN or chocolate agar
Pathogenesis
Type IV pili → initial adherence & antigenic variation (minicassettes)
Opa (P.II) proteins → tight binding, invasion, microcolony, phase variation
Porin P.I → pore formation, anti-phagocyte
LOS → TNFα release, strong neutrophil response (purulent exudate)
Sialylation of LOS → serum resistance, complement evasion
IgA1 protease, iron uptake from transferrin/lactoferrin
Clinical
Men: urethritis (purulent discharge, dysuria); 10\% asymptomatic
Women: cervicitis, urethritis; \tfrac{1}{3} asymptomatic; PID, ectopic pregnancy
Disseminated Gonococcal Infection (DGI) 1\text{–}2\% → arthritis-dermatitis, septic arthritis (knee)
Neonatal transmission → ophthalmia neonatorum
Treatment & Resistance
WHO surveillance: high quinolone resistance; rising azithromycin; emerging ESC resistance
CDC/MOH: single IM 250–500 mg ceftriaxone + azithro 1 g PO (cover Chlamydia)
Specimen & Diagnosis
Site-dependent swabs + first-void urine (NAAT)
Gram stain of male urethral pus: intracellular diplococci ★ rapid
Culture = gold standard (Thayer–Martin, 35–37^\circ\text{C}, 3\%–5\% CO₂)
NAAT (PCR/LCR), DNA probe ↑Sensitivity; blood/synovial culture for DGI
Chlamydia trachomatis
Biology / Life-Cycle
Obligate intracellular; biphasic life-cycle
Elementary body (EB) – infectious, metabolically inactive, disulfide-cross-linked wall
Reticulate body (RB) – non-infectious, metabolically active, replicates every \approx 3 h inside inclusion; cycles 7–21 d
Cannot synthesise ATP – “energy parasite”
Three biovars → serovars:
• Trachoma (A–C)
• Genital tract (D–K)
• LGV (L1–L3)
Clinical Spectrum
Genital chlamydia most common bacterial STI; 70\text{–}80\% women, 50\% men asymptomatic
Sequelae: PID, infertility, ectopic pregnancy, chronic pelvic pain, neonatal conjunctivitis/ pneumonia, HIV facilitation, cervical cancer link
LGV: transient genital ulcer → painful inguinal/femoral nodes (buboes), fistulae; ↑in HIV+ MSM
Diagnosis
First-catch urine or self-collected vaginal swab NAAT = sensitivity >95\% / specificity >99\%
Culture in McCoy cells (columnar epithelium) only \approx50\% sensitive
Cytology: inclusion bodies (Giemsa); serology for LGV
Therapy
Uncomplicated GTI: doxycycline 100 mg bid 7 d OR azithro 1 g single
LGV: erythro or doxy ≥21 d
Other Bacterial Ulcerative STIs
• Granuloma inguinale (Klebsiella granulomatis)
Painless, beefy-red ulcers; Donovan bodies on smear (Giemsa)
Treat doxy/azithro ≥3 wk until healed
• Chancroid (Haemophilus ducreyi)Painful soft chancre, serpiginous, purulent; unilateral tender nodes
Gram “school-of-fish” coccobacilli; culture on chocolate; treat azithro single dose or ceftriaxone IM
Fungal & Dermatophyte Conditions
Tinea cruris
Dermatophytes T. rubrum, E. floccosum → keratinase invasion of stratum corneum
Risk ↑ with moist/tight clothing; fomite spread; topical imidazole/allylamine
Candidiasis (Candida albicans)
Dimorphic yeast; commensal → opportunistic in immunosuppressed, diabetic, antibiotics, pregnancy
Genital ↓: cottage-cheese discharge; pruritus; balanitis in men
Culture: Sabouraud dextrose agar; CHROMagar speciation; treat topical azoles, nystatin (systemic fluconazole prn)
Parasitic STIs
Trichomoniasis
Trichomonas vaginalis trophozoites (flagellated) observed in wet mount
Frothy, foul discharge; strawberry cervix; treat metronidazole/tinidazole (both partners)
Pediculosis pubis & Scabies
Pthirus pubis – pruritic pubic lice; permethrin, malathion, nit combing
Sarcoptes scabiei – burrowing mites; intense nocturnal itch (type IV HS); topical permethrin or ivermectin PO
Pelvic Inflammatory Disease (PID) & Related Syndromes
Upper GT infection: endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis
Polymicrobial 30\text{–}40\%; key agents N. gonorrhoeae, C. trachomatis, anaerobes (Bacteroides, Peptococcus), G. vaginalis, streptococci, H. influenzae
Endometritis postpartum/abortion – mixed vaginal flora; historically S. pyogenes
Epididymitis <35 y: N. gonorrhoeae, C. trachomatis; ≥35 y: Enterobacteriaceae, staphylococci, corynebacteria
Epidemiology & Statistics
Incident curable STIs, adults 2020 (WHO):
• African Region 96\text{ M}
• Americas 74\text{ M}
• Europe 23\text{ M}
• Eastern Mediterranean 36\text{ M}
• South-East Asia 60\text{ M}
• Western Pacific 86\text{ M}
• Global total 374\text{ M}Global 2016 new cases (Rowley):
• Chlamydia 127\text{ M}
• Gonorrhoea 87\text{ M}
• Syphilis 6\text{ M}
• Trichomoniasis 156\text{ M}USA 2008 total prevalent STIs \approx 110\text{ M}; HPV highest 79\text{ M}
Malaysia studies
• Nordin 2001: Syphilis 50.8\%, Trichomoniasis 19.2\%, Gonorrhoea 8.5\%
• HKL 2013–17: Genital warts 26.7–45.6\% ; Herpes 11.8–31.5\% ; Syphilis ≈19\%; Gonorrhoea \le 12.2\%; Chlamydia 5.4\%; Trichomoniasis 0.2\%
Ethical & Practical Considerations
Asymptomatic carriage (e.g., Chlamydia, Gonorrhoea) drives silent transmission ⇒ routine screening in sexually active <25 y & pregnancy
Antimicrobial resistance (gonococci) demands stewardship, surveillance & novel therapeutics/vaccines
Congenital infections (syphilis, chlamydia, gonorrhoea) highlight importance of antenatal screening & treatment
Social stigma may delay care; patient education & confidentiality critical
Study Connections & Exam Tips
Compare pathogenesis strategies: stealth (T. pallidum) vs inflammatory overload (N. gonorrhoeae)
Recognise laboratory gold standards & rapid tests; match each pathogen with specimen type & media
Memorise treatment first-line drugs + resistance caveats
Link PID complications to infertility & ectopic risk – high-yield clinical scenario
Remember dermatological mimicry: painless (syphilis) vs painful (chancroid); indurated vs soft ulcer
Be able to sketch Chlamydia life-cycle & identify diagnostic window for serology vs NAAT
Selected References (See full list in transcript)
Rowley J. et al. Global & regional STI estimates 2016 — WHO
LaFond & Lukehart 2006. Biological basis for syphilis — CMR
CDC, WHO surveillance reports (Gonococcal AMR, syphilis maps)