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Sexually Transmitted Diseases (STDs)

Introduction Epidemiology
Genital Tract – Portal of Entry for Infection Diseases (Venereal, Non-Venereal) Global Estimates (WHO – 1999)
Venereal Disease = STD (includes all diseases spread by Sexual Intercourse)

Causative Agents
Bacteria
Treponema pallidum Syphilis
N. gonorrhoea Gonococcal urethritis
H. ducreyi Chancroid
Gardnerella vaginalis Bacterial vaginosis
Donovania granulomatis Granuloma inguinale
Chlamydia trachomatis NGU, Cervicitis, LGV
Mycoplasma genitalium NGU
Ureaplasma urealyticum NGU
Virus
HSV Genital herpes
HPV Genital warts (condylomata acuminate)
Hep. B Hepatitis
HIV AIDS
340 Million New Cases of STIs have occurred worldwide in 1999
Protozoa
Largest number of new infections occurred in region of
Trichomonas vaginalis Trichomonas vaginitis, NGU
• South, Southeast Asia
Others
• Sub-Saharan Africa
Fungi
• Latin America, Caribbean
Arthropods
Malaysia
Exact size of the problem is unknown
STD
• Underreporting
Spread through Sexual Contact – mucous membrane, breach in skin
• Underdiagnosis
Other Modes of Transmission
• Asymptomatic manifestation of disease
Mother-to-Child
• Existing Act (Prevention & Control of Infectious Act 1988)
• Pregnancy require notification of only Syphilis, Gonorrhea, Chancroid, HIV
• Delivery
• Reluctance to seek health care
• After Birth
• Most STD patients go to Private Doctors (not reported to MOH)
• Breast Milk (HIV only)
Transfusion or contact with Blood, Blood Products Epidemiology
STD Patients, especially ulcerative types
↑ Risk – Infected with HIV
(Require effe ctive, complete treatment of STD to ↓ HIV Risk)

Public Health Problem

Consequen ces - Health, Social, Economic
Serious Sequale
Pelvic Inflammatory Diseases
Impaired Fertility
Ectopic Pregnancy
Cervical Cancer
Affect Fetus, Infant
HIV Infection
Facilitate HIV transmission by
Incidence Rate of STD in Kelantan (2000-2004)
Disruption of Normal Epithelial Barrier by Genital Ulceration
STD 2000 2001 2002 2003 2004
Accumulation of pools of HIV susceptible, HIV-infe cted cells in
(Lymphocytes, Macrophages) Syphilis 2.87 1.41 1.26 1.3 0.74
Semen, Vaginal Secretion Gonococcal 1.71 0.82 0.37 0.9 0.61

Challenges Cases of STD Reported in Malaysia (1996-2000)

Asymptomatic (many cases)
Female (especially)
Continue to be infected, infectiou s to others
Reluctant to seek health care
Stigma
Lack of Con fidentiality, Privacy
Difficult to Notify Spouse, Sex Partner
Unavailability, Unsuitability of STD Services
Ignorance of STD
Causes, Symptoms, Cures, Conse quence s
Prescribed Treatment is substandard

Clinical Features
Vaginal Discharge Urethral Discharge +/- Dysuria (Male)
Trichomonas Vaginitis Gonorrhea
Vaginal Candidiasis Post Gonococcal Urethritis
Gonococcal Endocervicitis Non Specific Urethritis
Genital Ulcer
Syphilis
Chancroid
Genital Herpes
Neonatal Conj unctivitis
Gonococcal Conju nctivitis
Chlamydia Conjunctivitis
Bacterial Conjunctivitis
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Syphilis

Definition Classification
Communicable Disease, Caused by Treponema pallidum (Spirochaetaceae family) Primary Secondary Latent Late Congenital
Treponema = Turning Thread (Greek Term) Tertiary
Treponema pallidum Quaternary
Corkscrew appearance, 20 um in length, Moves in spiralling/ spinning motion Not all patients go through all these stages

Primary Syphilis (1°) Secondary Syphilis (2°) Latent Syphilis Tertiary Syphilis (3°) Congenital Syphilis
Pathogenesis Pathogenesis An Asymptomatic state Pathogenesis T. pallidum crosses Pacental Blood Barrier
T. pallidum enter body Develops 6-8 weeks after 1° manifestation (persist if Early Infection is not cured) After a Latent Period of 5-20 years or Longer Rapidly disseminate though out infected fetus
↓ ↓
Slow Tissue Damage ↓ Infection does not damage Fetus
Penetrating intact mucous membrane Due to Reaction of Circulating Spirochetes Represents a Hypersensitivity Reaction
↑ CSF Protein Level until 4th months of gestation
↓ with specific antibodies to small numbers of T. pallidum
Invading through epithelial abrasions Mild Pleocytosis (Treat Mother prior to this time can prevent
to form immune comple xes that Grow, Persist in Tissue
↓ Develop Late Manifestation of the disease congenital syphilis)
Grows, Multiplies in a Localized Area ↓ (symptoms depe nd on site of occurrence) Fetuses that acquire the infection
Spirochetes spread throughout the body (many patients - eventually) ↓
↓
↓ Non Contagious ↑ Mortality Rate
Spread to Lymph Node, Blood Stream Infectious Lesions occur on ↑ Destructive Phase (Stillbirth, Spontaneous Abortion)
Skin, Mucous Membrane All that Survive will develop
Incubation Period – 10 - 90 days (3 weeks) Skin, Mucous Membrane Lesi ons 1. Gummatous Syphilis (most common) Early, Late Congenital Syphilis
Typical 1° lesion (Chancre) Skin Lesions (can involve Palms, Soles) Develops in 15% of untreated cases Early Congenital Syphilis
A Single Painless Ulcer • Macular (within 1-10 years after infection) Occurs within 2 years
(with border, indurated base) • Papular Localized granulomatous lesion which Like severe Adult 2° Syphilis
Chancre represents an Intense Inflammatory • Occasional Pustular eventually Necrose, Fibrotic Widespread Rash, Condylomatum Latum
response to Bacterial Invasion • Nodular type rashes Mainly in Skin, Bones Enlargement - Lymph Node, Liver, Spleen
Patchy Alopecia Osteitis
Condylomata Lata
Mucous Patches
Mouth Ulcers

Chancre on Lower Lip

2. CVS Syphilis
Penile Chancre Occurs in 10% of untreated syphilis Osteitis
Painless Enlargement of Lymph Node (within 10-40 years after initial infection)
Extra Genital Chancre (5%) Systemic Symptoms Aneurysm of Ascending Aorta, Aortic Arch
Lips Fever, Rash, Generalized Lymphadenopathy, Necrosis of Media Layer of Aorta
Mouth Arthritis, Iritis, Retinitis Due to Chronic Inflammation of
Nipple Transmitted by Kissing (Extremely contagious) small arterioles supplying the aorta
Chancre disappears within 2-6 weeks Ulcer, Condyloma Lata Wall of Aorta Splits Late Congenital Syphilis
(whether or not Treatment is given) Lasts for Weeks → Months, Blood dissects through weakened media layer Similar to 3° Syphilis
then Gradually Subsides 3. Neurosyphilis Bone, Teeth (frequently involved)
Expressed in 8% of untreated cases Saddle Nose, Hutchinson’s Teeth, Saber Shins
(within 5-35 years of infection)
Manifested as - Meningitis, Meningovascular
syphilis, Tabes dorsalis, General Paresis, Argyll
Robertson Pupil
Argyll Robertson Pupil Hutchins on’s Teeth
Small, Irregular Pupils
Size may be unequal
Absence of light reflex
Prompt Accommodation
reflex
Pupils slowly dilate (with Saddle Nose
mydriatics) Saber Shin Oral, Skin Lesion
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Laboratory Test for Syphilis Interpretation of Serology Result
Direct Detection VDRL TPHA Interpretation
Dark Field Microscopy Almost Indicate Treponemal Infection
+ +
• Indicated in 1°, 2°, Early Congenital Syphilis Other Test Rarely Needed
• Specimen – Fluid (Exudate), Tissue from an open sore Probably Indicates biologically False +ve
+ -
(1° chancre, con dyloma latum, mucou s patch) Verification Test Indicated (eg. FTA-Abs)
Probably Indicate Old, Treated Infection
- +
Verification Necessary. False +ve TPHA < 2%
Syphilis Unlikely (FTA in suspected cases)
- -
Rarely Late, Early Primary Syphilis

Characteristics Serological Result

Clinical Specimen VDRL TPHA FTA Abs
A Lesion should be con sidered Non-Syphilitic only after 3 –ve examinations Primary Serum - or + - or + Usually +
have been made Secondary Serum Strongly + + +
Advantage Disadvantage Latent Serum Usually + + +
-ve results do not rule out syphilis Test does not work well on Late Serum - or + + +
Dry Sores Neurosyphilis CSF Usually + + +
Direct Detection Recent Treated Serum - or weekly + + +

Non-Venereal Treponemal Disease

3 Subspecies of pathogeni c T. pallidum causi ng diseases
Endemic Syphilis
Yaws Pinta
(Bejel)
Immunoflourescence T. pallidum subspecies T. pallidum subspecies T. pallidum subspecies
Electron Microscopy
pertenue endemicu m carateum
Serological Test
Cannot be distinguished
Screening Confirmatory
Non-Spe cific Specific • Serologically
Cardiolipin (Reagin) Antibody Test Treponemal Antibody Test • Morphologically
• Venereal Di sease Reference Laboratory • Treponema pall idum Haemagglutinatio n Have not been successfully Cultivated on Artificial Media
(VDRL) slide te st Test (TPHA)
• Rapid P lasma Reagin (RPR) te st • Treponema pall idum Part icle
• Automated Reagin Test ( ART) Agglutinati on Assay (TPP A)
• Toluid ine Red Unheated Te st (TRUST) • Fluorescent Treponemal Ant ibody
Absorpt ion Te st (FTA-Ab s)
• Microhaemagglutination assay for
antibodie s to Tre ponema pal lidum
(MHA-TP)
VDRL/ RPR TPHA
Screen for Syphilis Sheep RBC coated with T. Pallidum
Monitor Treatment are agglutinated by Patient’s Ab
Detect Ab to Cardiolipin in patients
with Syphilis
Done using
• Serum Sample FTA-Abs
• Spinal Fluid Test is more difficult to do
Not useful in Detects specific Antibodies to
• Very Early Detection bacteria that cause Syphilis
• Advanced Stages Syphilis Can detect Syphilis in All Stages
False +ve Cardiolipin Test (except during 1st 3-4 weeks)
• Infectious mononu cleosis Done using
• SLE • Blood Sample
• Viral Pneumonia • Spinal Fluid
• Pregnancy
• Narcotic addiction
• Autoimmune diseases
• Leprosy
• Malaria
• Vaccination
Isolation of Treponema pallidum
T. pallidum cannot be cultivated on artificial media
Inoculation of Lab oratory Animals (Higher Primates, Rabbit Testes) is the only
mean presently available to isolate organism

Treatment
Penicillin – Treatment of choice for all form of Syphilis
Alternatives if Patients Allergic to Penicillin
Tetracycline
Doxycycline
Erythromycin
Jarisch-Herxheimer Reaction
Inflammatory response to Spirochete Antigen
Occurs within hours of 1st Antibiotic Dose with
• Fever
• Exacerbation of Inflammation
Can be Minimized by starting ↓ Dose Penicillin or adding Corticosteroid
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Gonorrhoea Chlamydia Trachomatis

Definition Definition
Neisseria gonorrhoea (GNDC, intracellular) Very small bacteria, Obligate Intracellular Parasite
Incubation – 1-10 days Can exist in different forms
Clinical Features Elementary Body (EB) Reticulate Body (RB)
Urethritis Adapted for Extracellular Survival Adapted for
Rectal gonorrhoea Initiation of Infection Intracellular Multiplication
Pharyngeal gonorrhoea
Complications
Prostatitis
Epididymo-orchitis
Bacteraemia
Skin Rash
Septic Arthritis
Ophthalmia Neonatorum Gonorrhoea
PID Discharge (Pus) from Penis Clinical Presentation
Lymphogranuloma Venereum (LGV)
Female Male
Urogenital Infection (NGU)
Majority Asymptomatic Majority Symptomatic
Ocular Trachoma
(Reservoir)
Perinatal Infection
Pathogenesis
Gonococci attach to Persistent Untreated Infection Lymphogranuloma venereum (LGV)
Chlamydia trachomatis serovars L1, L2, L3
Mucosal Cells by means of Pili Chronic Inflammation (topical countries)
↓ Fibrosis ↓
Bacteria rapidly Multiply 1° Lesion
Spread through Cervix Painles s, Small Genita l Ulcer
(passes u nnoticed at site of in oculation)(incubat ion 1-4 weeks)
Up the Urethra in Men ↓
↓ Lesion heal s rapi dly
Inflammation ↓
Chlamydiae proceed to infect dra ining Lymph Node
Pus Formation ↓
Painful En larged Inguinal Nodes
↓
Virulence Factors Multip le Abscess Format ion
Pili ↓
Ruptured
Adherence to Epithelial cells ↓
Mediate resistance to Phagocytosis Extensive Ulceration to Genital ia
Pelvic Infection
Outer Membrane Protein
↓
Antigenically variable, Expressed by strains that Resist Serum Killing Years later, Perinea l, Inguinal Fi bros is occur
Cause Disseminated Gonococcal Infe ction (usually) Rectal Stricture, Genital Lymphoedema

Others
1° Genital Ulcer does not coexist with Lymph Node enlargement
Lipooligosaccharide (LOS)
IgA
Protease
Capsule

Genital Lymphoedema Groove Sign (man with LGV)

Treatment
Doxycycline (100mg bd for 3 weeks)

Urogenital Infection (NGU)

Thinner Mucoid Purulent Urethral discharge
Clinically impossible to differentiate from Gonorrhoea (some mixed infe ction)
Chlamydial NGU does not respond to Penicillin
Lab Diagnosis
Laboratory Diagnosis Specimens - Urethral discharge, Endocervical scraping, Urine
Specimen Microscopy Examination Direct Detection from Antibodies
Antigen Detection
Urethral discharge Gram-stains Urogenital Specimen Detection
Cervical, Pharyngeal, Rectal Swab GN Diplococci Intracellular Specific IF monocl onal Rapid antigen assay Complement
Blood Cultures in Pus cells antibody of Chlamydia Immunochromatography Fixation Test
Gonococci rapidly died on swab (Glass slide) EIA Culture
(unless suitable transport medium) • McCoy,
(Amies medium) • Chic embryo
Culture tissue
Chocolate Agar PCR
Selective Media • Urogenital
DFA (Direct Fluorescent Assay)
Thayer Martin VCT Agar specimen
Gonorrhoea +ve -ve
Added CO2 • Urine
≥ 10 EBs Free of EB
Rectal Swab in Female – 40-60% +ve At least 10 columnar cell
Blood Culture indicated in present
Gonococcal Epididymo-orchitis
PID
Skin, Joint Infection

Treatment Iodine Stain

IM Ceftriaxone 125mg (single dose) Presence of
Penicillin G Inclusion Body in cell
↓ Sensitivity (due to Penicillinase producing Gonococcal Strains) Treatment
Doxycycline, Azithromycin Doxycycline (100mg bd for 7 days)
Treat for C. Trachomatis (50% of patients concurrently infected) Abstinence Sexual Intercourse during treatment
Alternative – Azithromycin (1gm single dose orally)
Follow up of treated cases for at least 3 months
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Viral Infection Parasites Infection
Herpes Simplex Virus Trichomonas vaginalis
Human Papilloma Virus Scabies (Sarcoptes scabiei)
Human Immu nodefi ciency Virus (HIV)* Ptriasis pubis
Hepatitis B Virus*

Herpes Simplex Virus Trichomonas vaginalis

Definition Definition
HSV-1 HSV-2 Trichomoniasis
Spread by contact – Infected Saliva Transmission Trichomonas vaginitis
Associated with Sexually Urethritis (NGU) (occasionally)
Oropharyngeal lesions Maternal genital infection – newborn Copious Watery Frothy vaginal discharge with Offensive Smelling
Recurrent attacks of Fever Blisters 1° infects genital mucosa Associated with
(Cold Sores) Genital Herpes Vulva irritation
Oral Herpes Dysuria
Can also cause Ge nital Herpes Dyspareunia
Orogenital contact Abdominal Pain
Can Cause Male Partner – Asymptomatic
Neurologic disease Can Infect Neonates – during passage through an infected birth canal
Severe Neonatal Herpes Infection
Examination
Clinical
1° Illness - Can be severe (lasting 3 weeks)
Vesico-ulcerative lesions
Lesions
Very Painful
Associated with
Fever
Malaise
Dysuria
Inguinal Lymphadenopathy Erythematous, Purulent Frothy Strawberry appearance (mucosa )
Cluster of Vesicles Vaginal Discharge Mucosal capillary dilatation
Break Down Vulva, Vestibular, Vagina
↓
Painful Ulcer
↓
Laboratory Diagnosis
2° Infection Fluid from Posterior Fornix for
Viral Excretion persists – 3 weeks immediate Wet Mount by microscopy
Recurrences of genital herpetic infections • Protozoa larger than Leukocyte
• Common • Pear shape
• Tend to be Mild, Asymptomatic • Motile
HSV-2 Recurs ↑ often than HSV-1 • Flagellated
Urine
Laboratory Diagnosis
Direct Microscopy Treatment
Specimen – scrapings from base of vesicle Metronidazole
Stain with Wright, Giemsa (Tzanck smear) Treat partner regardless of symptoms
Quick results (cannot differentiate HSV-1 from HSV-2) (if not recurrence may occur)
Viral Culture from Vesicle Material
Gold Standard
Antigen Detection
EIA
IF
Antibody Detection
EIA
PCR

Treatment
Acyclovir (viral DNA synthesis Inhibitor)
May
Suppress Clinical Manifestation
↓ Time to Healing
↓ Recurrences
HSV Latent in sensory ganglia cannot be eliminated
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Prevention of STD
Primary (1°) Secondary (2°) Tertiary (3°)
↑ Health promotion behaviour Screening Treat Complication that arose
Education Asymptomatic persons (↑ Risk STD) Palliative care for terminally ill
Promotion • Multiple Sex partners
Promote Healthy Lifestyle • History of STDs
Safe Sexual Practice • Sex partner that has multiple sexual contacts
Barrier method (Condom) (known, suspected to have STD)
HSV, HIV, Hep B Virus Antenatal Mothers
Sex Education in Schools Health Care
Vaccination ↑ Accessibility, Affordability to Health Care
Hepatitis B Virus (the only one available) ↑ Competencies to early diagnosis, treatment
(Health Staff)
Prompt Treatment
Partner Notification, Management
Done in 1° and 2° STD Prevention
Primary (1°) Secondary (2°)
↓ Risk of acquiring Infected Sex Partners can
infection by uninfected receive prompt medical
partners treatment
Changing Behaviours