Week 4 reproductive system

L25 - Disorders of sexual differentiation

Genetic causes of infertility
Male infertility causes Female infertility causes

- Chromosomal abnormalities (Kleinfelters 47XXY) - turner syndrome (45, XO)

- Y chromosome micro deletions - Fragile X pre-mutation (repeat expansion) (FMRI,
- Mutations a ecting spermatogenesis (e.g CFTR Fragile X mental retardation gene(
mutations in CBAVD, Congenital bilateral - Mutation in genes regulating ovarian function &
absence of vas deferens) meiosis
• Most men with CBAVD carry mutations in CFTR
gene
Y chromosome micro-deletion
- small deletion on Yq (long arm) -> major genetic cause of male infertility
Important regions (Azoospermia factor)
- AZFa -> cause sertoli cell only syndrome (sertoli cell remain but no germ cells (sperm
precursors)
- AZFb -> cause spermatogenic arrest
- AZFc -> cause oligo/azoospermia (most common)
Detected by
- PCR based genetic testing
- Important for assistive reproductive technology (ART)
Levels of sex determination
Chromosomal sex - determined at fertilisation by sex chromosomes
e.g
- XX (female)
- XY (male): variations XO (turner), XXY (kleinfelter)
Gonadal sex - determined by type of gonads that develop from undi erentiated gonad
e.g
- Testes (with SRY/TDF)
- Ovaries (without SRY)
Phenotypic sex - determined by physical characteristics of internal + external genitalia and
later secondary sexual trains
e.g
- Penis, vagina, body hair, breast development, voice changes
Key genes in sex determination
SRY gene
Mutations
- Absent/mutated SRY on Y -> XY female (looks female but with XY)
- SRY translocated to X -> XX male (looks male despite XX)
Other genes involved
SOX 9
- acts downstream of SRY, helps reinforce testis formation
DAX 1 (on X)
- promotes ovarian pathway, if duplicated XY can ip to female (sex reversal)
WNT4, FOXL2
- important for ovary development
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 Gonadal di erentiation
Male gonadal di erentiation Female gonadal di erentiation

1. Primordial germ cells migrate to genital ridges 1. Primordial germ cells migrate to genital ridges
(week 4-5) -> biopotential gonads form (4-5 weeks)
2. SRY on Y chromosome produces TDF -> 2. Absence of SRY -> no TDF -> gonads
initiates testis development di erentiate into ovaries
3. TDF -> formation of sertoli cells -> secretion of 3. Ovarian cords form and give rise to primordial
AMH (anti-mullerian hormone) -> regression of follicles
mullerian ducts (female pathway blocked) 4. Germ cells di erentiate into oogonia
4. Sertoli cells signal leydig cells to form -> 5. No AMH -> mullerian duct persists into uterus,
produce testosterone -> development of fallopian tubes, cervix and upper vagina
woll an ducts into epididymis, vas deferens, 6. In absence of testosterone/DHT -> woll an duct
seminal vesicles regress -> female development pathway
5. Testosterone -> DHT : develops male external (clitoris, labia, lower vagina)
genitalia + prostate 7. Middle + caudal part of mullerian ducts undergo
median migration and fusion
- cranial 1/3: tubes
- Middle 1/3: uterus + cervix
- Caudal 1/3: upper 3/4 of vagina
Phenotypic di erentiation
Undi erentiated stage
- before week 8 of gestation urogenital tract looks identical in both sexes
- Structures present
• Genital tubercle
• Genital (urethral) folds
• Genital swelling
Male phenotypic di erentiation
Androgen ->
- masculinisation of external genitalia (12th-13th week)
- Penile growth + testicular descent (3rd trimester)
Female phenotypic di erentiation
- absence of circulating testosterone maintains appearance of female external genitalia at 6th
week gestational stage
Brain phenotypic di erentiation
Male: under testosterone + DHT in uence Female brain: without early testosterone
exposure

Brain masculinisation occurs when testosterone Absence of testosterone during critical fetal stages
(from fetal testes) crosses blood brain barrier -> brain feminisation
Structural di erences Estrogen levels rise only later (puberty)
- pre optic area of hypothalamus (responsible for Structural di erences
thermoregulation) larger in males - some hypothalamic nuclei smaller than males
- Amygdala (important for aggression + emotion) - Corpus callosum + anterior commissure may
tends to be more active + structurally di erent show inter hemispheric connectivity
Functional di erences Functional di erences
- More lateralisation (stronger division of tasks - greater bilateral activation for certain cognitive
between hemispheres) tasks
- Tendency towards spatial skills, motor - Enhanced verbal ability, memory and social
coordination and systemising behaviours cognition
Behavioural outcomes Behavioral outcomes
- higher drive for competition, risk taking and - stronger orientation towards empathy,
sexually dimorphic behaviours communication and nurturing behaviours
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 Gender identity
- identi cation of self as either female or male (internal sense) + distinct from biological sex
(determined by chromosomes gonads and genitalia)
- Prenatal androgen levels shape brain development -> in uence male or female typical
behaviours + gender identity
- Post natal environmental factors + learning (social etc) have important e ect
Transgender
- people whose gender identity is di erent from sex they were assigned at birth
Disorders of sexual di erentiation
1. Seminiferous tubule dysgenesis
a. Klinefelter syndrome
- most common DSD
Genotype - Genotype: Male with at least 1 Y + 2X chromosomes
- Classical: 47 XXY
- Variants: 48 XXXY/48XXYY
Cause - Nondisjunction during meiosis (in either parent)
Gonads - small rm atrophic testis, small number of leydig cells, azoospermia
except in mosaic
Hormones • Low-normal testosterone
• Increase FSH, LH, Estrogen
Phenotype • normal male
• external genitalia not ambiguous
• Taller than average
• Reduced facial hair + body hair
• Gynecomastia
• Feminine fat distribution
• Osteoporosis
• Testicular atrophy
• Varicose veins
Diagnosis • Karyotyping to con rm extra X chromosome
• Hormone tests: low testosterone, high FSH + LH
• Physical examination + medical history
Complications • High incidence of breast cancer (x8).
• Predispose to Sertoli and Leydig cell tumour.
• Infertility.
Management 1. Androgen replacement (induce/maintain secondary sex characteristics)
2. Surveillance for testicular tumour + breast carcinoma
3. Fertility options: assisted reproductive techniques if sperm present
4. Speech, occupational, or educational support for learning di culties.
5. Psychological counselling if needed.
b. 46XX male
Cause Due to translocation of Y chromosomal material, including SRY (TDF) to the X
chromosome
Gonads - small rm atrophic testis, small number of leydig cells, azoospermia
Hormones - Low testosterone (testes underdeveloped)
- FSH, LH, estrogen increase
Complications - same as Klinefelter but shorter + normal skeleton proportions & mild or no learning
issues
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2. Syndromes of gonadal dysgenesis
a. Turner syndrome
Incidence 1:2500 live births

Genotype 45 XO
Mosaics: (45XO/46XX, 45XO/46XY)

Gonads Fibrous streaks (no surviving germ cells)

Hormones Decrease in androgen + estrogen

Increase in FSH + LH

Phenotype - Normal female external genitalia, not ambiguous

- Renal abnormalities 33% (structural or positional)
- Kidney or renal agenesis + malrotation
Diagnosis - Karyotype analysis (de nitive, prenatal detection by amniocentesis or chronic
villus sampling)
- Hormone testing: low estrogen, high FSH/LH
- Ultrasound: heart/kidney abnormalities
Clinical features - short stature
- Webbed neck, low hairline, broad chest with widely spaced nipples
- Streak ovaries -> primary ovarian failure ( brous CT)
- Amenorrhea (absence of menstruation) + infertility
- Lymphedema in hands/feet at birth
- Normal intelligence (but possible di culties in math/spatial reasoning)

Complications - CVS: coarctation of aorta, bicuspid aortic valve, hypertension

- Renal malformations
- Osteoporosis due to estrogen de ciency
- Infertility
- Hearing loss, thyroid disorders (autoimmune)

Management - growth hormone therapy in childhood to improve height

- Estrogen replacement therapy: induce puberty + maintain bone/heart health
- Fertility counselling: IVF with donor oocytes
- Regular monitoring + treatment of cardiac renal, thyroid and bone health
- Educational + psychological support
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 Gonadal dysgenesis
Pure Mixed Partial

Karyotype 46XX or 46XY (Swyer) 45X/46XY mosaic 46XY

Gonads Bilateral streak gonads 1 side dysgenic testis 1 side 2 gonads partially
streak gonad developed
Dysgenic testis (often intra- Underdeveloped testicular
abdominal) tissue
- produce AMF -> regression of
mullerian ducts
- Produce testosterone ->
promote ipsilateral woll an
duct di erentiation
Contralateral streak gonad
- no MIS and testosterone
produced -> mullerian duct
di erentiate (uterus + fallopian
tube) + no woll an duct
development

External Female Ambiguous (female -> Ambiguous (undervirilised

genitalia Not ambiguous undervirilised male) male, clitoromegaly,
hypospadias)

Hormones Low estrogen/ Variable Variable: partial androgen

testosterone Some testosterone from production
High FSH/LH dysgenic testes

Puberty No spontaneous puberty Variable, may need hormone Incomplete/delayed

therapy puberty

Fertility Infertile Usually Infertile Usually infertile

Tumour risk 46XY: high -> High (dysgenic testis with Y Moderate, depending on
gonadoblastoma material) dysgenic tissue

Mangment N/A Gender assignment depends on

external genitalia + gonads
If gender assigned female
- orchidectomy (prevent cancer)
+ hormone replacement
If gender assigned male
- orchiolysis (free testes from
abnormal attachment)
- Or gonadectomy + androgen
replacement to induce +
maintain male secondary
sexual characteristics
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 3. Bilateral vanishing testis/testicular regression syndromes
- 46XY
- Absent testis with clear evidence of testicular function at some point during embryogenesis
- Due to genetic mutation, teratogen, or bilateral torsion
- Diagnosis: Elevated FSH/LH & castrate (very low) testosterone levels
3 phenotypes according to time vanishing occur
Most severe Intermediate Least severe

- before 60-70 days gestation - after liberation of MIS + - late after complete anatomic
- MIS secreted but before incomplete eloberation of development of male external
elaboration of androgen androgen genitalia
- Phenotypic female with no - Ambiguous genitalia, absent - Phenotypic male with fully
internal genital structures gonads, internal ductal develop woll an structure but
(testicular regression structures empty scrotum + microphallus
syndrome) (bilateral vanishing testes
syndrome)

True hermaphroditism (Ovotesticular)

- both testicular + ovarian tissue either in separate gonads or coexisting in same gonad as
ovotestis
- Karyotype variable not helpful for diagnosis
- Phenotype: ambiguous genitalia with tendency of masculinisation (75% raised as male)
- Internal organs variable + according to present gonad
- Pregnancy documented in female only
Management
- gender assignment based on functional potential of external genitalia, internal ducts and
gonads according to ndings done by laparoscopy or laparotomy
- If patient raised as female: testicular + woll an tissue removed
- If patient raised as male: ovarian + mullerian tissue removed
- Gonadectomy at puberty with high androgen replacement due to high risk of malignancy + no
hope for fertility

Female pseudohermaphrodite (Masculinised female)

- 46XX karyotype + ovaries, but ambiguous/masculinised genitalia
- Gonads: normal ovaries (internal female reproductive organs)
- Cause:
• Excess androgen exposure during fetal development
• Most common: CAH - 21 hydroxylase de ciency (phenotype depends on severity of enzyme
de ciency)
• Other causes: maternal androgen exposure, virilizing tumours
- Phenotype
• Enlarged clitoris (cliteromegaly)
• Labial fusion
• Partially masculinised external genitalia
• Normal uterus + fallopian tubes
- Diagnosis
• Karyotype: 46XX
• Hormonal studies: elevated androgens (17-OH progesterone in CAH)
• Ultrasound: normal internal female organs
- Management
• Glucocorticoid therapy in CAH to reduce androgen excess
• Surgical correction of external genitalia if needed
• Fertility counselling: ovaries usually functional
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 Male pseudohermaphrodite (undermasculinised male)
- 46XY karyotype + testis with ambiguous or undervirilised external genitalia
- Gonads: testes (may be undescended or dysgenic)
- Causes
• Androgen biosynthesis defects (e.g 5a-reductase de ciency, 17b-hydroxysteroid
dehydrogenase de ciency)
• Androgen insensitivity syndrome (partial): inability of target tissue to respond to androgen
• Leydig cell hypoplasia
- Phenotype
• Micropenis
• Hypospadias
• Bi d scrotum (scrotum split into 2 halves) or partially fused labioscrotal folds
• Undescended testes
Classi cations
1. Leydig cell aplasia
2. Disorders of testosterone biosynthesis
3. 5-a reductase de ciency
4. Androgen receptor + post-receptor defects (testiular feminisation)
5. Persistant mullerian duct syndrome (hernia uteri inguinale)
Karyotype: 46,XY
External Genitalia: Normal male
Internal Genitalia: Presence of Müllerian duct structures (uterus, fallopian tubes, upper vagina)
Testes: Often unilateral or bilateral undescended testes (cryptorchidism)
Diagnosis: Commonly identi ed when Müllerian tissue is found during inguinal hernia repair
(herniorrhaphy) or orchidopexy
Treatment
• All patients are phenotypic males, so orchidopexy is the main treatment.
• During surgery, care must be taken to preserve the vasa deferentia, which lie close to the
uterus and proximal vagina.
• Preservation of Müllerian structures is recommended if their removal risks damaging the
vasa, in order to preserve fertility.

L26 + 27 - STD 1 & 2

Causative agents of STI’s
Syphilis Treponema Pallidum

Chancroid Haemophilus ducreyi

Genital herpes Human herpes virus

Lymphogranuloma venereum Chlamydia trachomatis

Donovanosis Klebsiella granulomatis

Treponema Pallidum (Syphillis)

- slender spirochetes with ne spirals and pointed ends
Stages of disease
Initial contact (2-10 - Primary chancre at Pathogenesis:
weeks) + site of infection - multiplication of
Primary syphilis (1-3 - Enlarged inguinal treponema at site of
months) nodes, spontaneous infection
healing - Proliferation of
treponema in regionial
lymph nodes
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 Secondary syphilis 2-6 - u like illness: - multiplication + Skin rash
weeks myalgia, headache, production of lesion in
fever, mucocutaneous lymph nodes, liver,
rash joints, muscle, skin and
- Spontaneous mucous membranes
resolution

Condyloma lata

Mucosal patch

Latent syphilis (3-30 Treponema’s dormant in

years( liver or spleen
Re-awakening and
multiplication of
treponema

Tertiary syphilis - neurosyphilis: general - further dissemination Gumma

paresis of insane and invasion of host
- Tabes dorsalis response (cell
- Cardiovascular mediated
syphilis: aortic hypersensitivity)
leisions, heart failure - Gumma in skin,
- Progressive bones, testis
destructive disease

Gumma
Congenital syphilis
- transmission to fetus from mother experiencing primary/secondary syphilis -> often results in
death of fetus
- If transmission occurs while mother is in latent phase of disease, fetus su ers mental
retardation + malformation of organs
- After birth: newborns with latent infections exhibit widespread rash like that of secondary
syphilis at some time during their rst 2 years of life
Diagnosis
Microscopy Dark eld microscopy of Fluorescent labeled Silver impregnation
lesions [Link] Antibodies method
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 Serology (antibody detection)
Nontreponemal tests
Reagin antibodies detected by using cardiolipin antigen
1. Venereal disease research laboratory (VDRL) test
2. Rapid plasma reagin (RPR) test
- measure IgG or rarely IgM Abs (reaginic antibodies against lipids released from damaged cells)
- Antigen in test: cardiolipin (diphosphatidyl glycerol) from beef heart
- Antibodies form in serum 2-3 weeks after infection
- Cheap tests but false positive results (Malaria, infectious mononucleosis, SLE, relapsing fever,
malaria, viral hepatitis, HIV, pregnancy and IV drug abusers)
Treponemal tests
- used to con rm positive VDLR/RPR tests
Types
- FTA-ABS ( uorescent treponemal antibody absorption test)
- THPA (T pallidum hemagglutination test)
- TPI (treponema pallidum immobilisation test)
- TPA (T pallidum agglutination test)
- TPPA (T pallidum particle agglutination test)
- Remains positive for life
- T pallidum cant be cultured in vitro
Genital ulcers - Chancroid (soft sore) - Haemophilus ducreyi
- pleomorphic gram negative coccobacillus
- Occurs in groups/in parallel chains
- Bipolar staining (school of sh/railroad track appearance)
- More common in developing countries
- Strong association with HIV infection
Clinical features
-papule on genital area erodes and form painful non indurated ulcer
with ragged edges + yellow exudate at base
-Associated often with painful enlargement of local lymph nodes
(bubo)

Diagnosis

-direct gram lm of exudate form chancroid: slender gram negative bacilli in

school of sh arrangement
-Culture: requires enriched media (rabbit blood agar, selective media with
growth factor X = heme)
-Molecular tests: PCR (highly sensitive)

Genital ulcers - Human herpes virus (HHV)

- Enveloped polyhedral linear double stranded DNA viruses
- HSV-2 = 85% of genital herpes
- HSV1= cold sore virus -> usually via oral-genital contact
Clinical presentation
- genital ulcers (multiple, painful, tiny vesicular ulcers, often bilateral and widely spread)
- Inguinal lymphadenopathy (enlarged, tender, rm, commonly bilateral)
Latency and recurrence
- HIV remains latent in sensory nerve ganglia and can reactivate (triggered by stress, fever or
immunosuppression)
• HSV-1: latency in trigeminal ganglion -> oral herpes recurrences
• HSV-2: latency in sacral ganglia -> genital herpes recurrences
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 Lab diagnosis

-Staining of scrapings from base of lesions with giemsa’s (tzanck

preparation) or papanicolaou’s stain can detect multinucleate giant
cells or intranuclear inclusions of HSV infection
-Detection of herpes virus DNA by PCR
-Viral antigen = identi ed by direct immuno uorescent staining of
infected cells or by using ELISAs

Granuloma inguinale (Donovanosis) - klebsiella granulomatis

- intracellular gram negative bacterium
Clinical features
- painful slow progressive ulcerative lesion that is highly vascular +
PAINLESS
bleed easily on contact
- On genitals or perineum
- Lymph node involvement is rare however pseudobuboes may be
seen in inguinal region in 10% of cases
Lab diagnosis
- Donovan bodies seen as large cyst like macrophages lled with deeply
stained capsulated bacilli having a safety-pin (bipolar) appearance

- non motile, capsulated and gram negative bacilli

- PCR

Chlamydia trachomatis
- 2 morphologically distinct forms
- Cannot be cultured
- Obligate intracellular parasites
- A nity for squamocolumnar epithelial cells (cervix, urethra, rectum, conjunctiva)
Life cycle
1. Attachment & uptake: infectious elementary body attaches to host cell and is endocytosed
2. Transformation: elementary body converts to reticulate body (metabolically active form)
3. Replication: reticulate body divides by binary ssion forming inclusions within host cell
4. Conversion: reticulate bodies convert back to elementary bodies
5. Release: host cell releases elementary bodies which infect new cells
6. Persistent infection: sometimes reticulate bodies persist as large aberrant forms -> chronic
infection
7. Cycle continues
Serotypes and associated disease
A,B,C
- trachoma (chronic eye infection -> blindness in endemic areas)
D-K
- genital infectons: cervicitis, urethritis, PID, proctitis, neonatal
conjunctivitis, neonatal pneumonia
L1,L2,L3
- lymphogranuloma venereum (LGV)
• Initial transient genital ulcer
• Followed by tender inguinal lymphadenopathy (groove sign)
• Incubation: 3 days -> 6 weeks
• Features: Rectal strictures, rectovaginal or rectal stulae, edematous
granulomatous hypertrophy of vulva scrotum or penis, chronic lymphedema -> elephantiasis
of vulva or scrotum
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 Stages of lymphogranuloma venereum (chlamydia trachoma’s serovars L1-3)
Stage 1 Primary lesion
- painless ulcer/papule on penis, vulva, cervix or rectum
- Lesion heals spontaneously and may go unnoticed
Stage 2 Inguinal stage
- regionial inguinal lymphadenitis (bubo)
- Nodes enlarged, tender and may become uctuant
- Buboes can rupture -> chronic stulae with external discharge
Stage 3 - seen in untreated cases
- Especially in women and men that have sex with men

Urethritis
- in ammation of urethra
- Urethritis in men produce urethral discharge + dysuria, usually without frequency of urination
Gonococcal urethritis (Neisseria gonorrhoea)
Lab characteristics
- gram negative intracellular
diplococci (bean shaped)
- Specimen is from urethral,
vaginal, cervical and anal
exudates
- Abundant pus cells
- In females only 50% sensitive
because they carry neisseria in
normal ora

Labs - positive catalase and oxidase

- Carbohydrate utilisation
- Glucose +ve (produce acid)
- Maltose -ve
- Nucleic acid ampli cation tests (NAAT)
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 Culture
- modi ed Thayer Martin agar
(chocolate agar + antibiotics:
vancomycin, colistin, nystatin)

Virulence factors - pili or mbriae: adhesion + prevent phagocytosis

- Outer membrane proteins (Porin/protein I), 2 types
• PorB 1A = associated with disseminated infection
• PorB 1B = localised urogenital infections
- Opacity associated protein (protein II): Adhesion to neutrophils
- Lipo-oligosaccharide (LOS): endotoxin
- IgA1 protease: break down secretory IgA
- Transferrin binding + lactoferrin binding proteins acquire iron from
host

Clinical disease Males

- acute urethritis: purulent urethral discharge, dysuria
- Complications: epidiymitis, prostatitis, periurethral abscess
Females
- less severe -> asymptomatic carriage common
- Mucopurulent cervicitis
- Vulvovaginitis
- Spread to adjacent organs -> bartholinitiis, salpingitis, PID
- Fitz-Hugh-Curtis syndrome -> rare complication, peritonitis with
peri-hepatic in ammation
Both sexes
- anorectal gonorrhoea (proctitis)
- Pharyngeal gonorrhoea (pharyngitis)
- Ocular gonorrhoea (conjunctivitis)
Pregnancy
- adverse outcomes: prolonged rupture of membranes, premature
delivery, chorioamionitis, maternal sepsis
- Infant at risk of infection during delivery
In neonates
- ophthalmia neoinatorum (purulent conjunctivitis, may lead to
blindness -> treat with erythromycin eye drops)
Disseminated gonococcal infection (DGI)
- polyarthritis, rarely dermatitis, endocarditis
HIV infected persons
- gonorrhoea increases HIV transmission 3-5 fold due to mucosal
in ammation + shedding
Non-gonococcal urethritis (NGU)
Bacteria
- Chlamydia trachomatis (D-K) - Most common agent, obligate intracellular parasite)
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 - Genital mycoplasmas: ureaplasma urealyticum, mycoplasma genitalium, M hominis
- Spherical to lamentous cell with no cell walls
- Attachment organelle at tip of lamentous M pneumoniae + m genitalium and other
pathogenic mycoplasmas
- Fried egg shaped colonies on agar
- Mycoplasmas = require cholesterol for growth
- Ureaplasma = require urea for growth
Epidemiology - frequently colonise lower urogenital female tract

Transmission - sexual contact mainly

- Mother-fetus transmission during childbirth
Clinical manifestations Non-gonococcal urethritis (NGU):
• Commonly caused by M. genitalium and Ureaplasma.
Epididymitis:
• Associated with M. genitalium and Ureaplasma.
Pelvic In ammatory Disease (PID):
• Mainly caused by M. hominis.

Diagnosis - Culture (di cult as ureaplasma form tiny colonies)

- PCR -> most sensitive + speci c
Virus
- Human herpes virus (HSV-1,HSV-2) - mainly [resent as genital ulcer but can also cause
urethritis
Fungi
- Candida albicans - in addition to urethritis also causes vulvovaginitis
Parasites
- Trichomonas vaginalis - in addition to urethritis also cause vulvovaginitis

Genital TB (M tuberculosis)
- more common in female
- A ect fallopian tube and endometrium -> cause infertility, pelvic pain, menstrual
abnormalities and adnexal swelling
- endometrial biopsy: show tuberculous granulomas
- In Male:
- Genital TB mainly e ects epididymis -> produce slightly tender mass that may drain
externally through stulous tract
- Other manifestations: orchitis + prostatitis
Genital warts (HPV 6 + 11)
- benign tumours of squamous cells
- surface smooth or rough
- HPV 16 + 18 commonly associated with anogenital neoplasia
Transmission
- skin to skin contact + genital contact
Lab
- Koilocytes
- In women: pap smear to screen for cervical cancer
- PCR
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 Proctitis
- caused by HHV, neisseria gonorrhoea, C trachomatis
Vulvovaginitis
- in ammation of vaginal mucosa (vaginitis) + external genitalia vulva (vulvitis)
- Symptoms: vaginal symptoms e.g abnormal discharge with/without o ensive odour or itching
Common cause in premenopausal women
Trichomoniasis
(Trichomonas
vaginalis)

- strawberry cervix (with

petechiae)
- inhabits vagina in
women
- Inhabits urethra +
sometimes prostate in
men
Infected women
- foul smelling, yellowish
green vaginal discharge
- Vaginal irritation
- Increase in vaginal pH
Direct microscopy Culture Molecular methods
- wet (saline mount): jerky - gold standard - PCR (highly sensitive
motile trophozoites + - Detects low parasite + speci c)
pus cells loads better than Other diagnostic clues
Permanent stains microscopy - pH of vagina >4,5
- giemsa, papanicolaou Antigen detection - Positive whi test:
stain - rapid add 10% KOH to
Fluorescent stain imunochromatographic vaginal discharge ->
- acridine orange test (ICT) shy odour due to
- Direct uorescent - ELISA (detect amine production
antibody test antibodies but less
commonly used, not as
speci c

Candidal Opportunistic infection Clinical features - gram stain: gram +ve

vulvovaginitis - long term antibiotics - perivaginal pruritus yeast like cells with
(Candida albicans) - Suppression of normal (itching) budding
ora - Erythema + vaginal pseudohyphase
- Immunocompromised discharge - thick and Culture
patients cheesy (cottage - sabarauds dextrose
cheese) with pH <4.5 medium
- White adherent - Germ tube positive
membranous patches
in vagina with itching +
irritation
Bacterial vaginosis
- increased homogenous white discharge from vagina + malodour (rotten shy smell)
Causative agents
- gardenerella vaginalis
• Normally present in low numbers in genital tract but in BV outnumbers other organisms
• Gram negative, non motile pleomorphic bacilli
• Shows metachromatic granules
- Mobiluncus sps
• Motile curved gram variable or gram negative anaerobic rods
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 - Mycoplasma hominis
- Prevotella sps
- Ureaplasma urealyticum
- Peptostreptococcus
Pathogenesis
- Loss/reduction of normal vaginal ora (lactobacillus acidophilus, L jenseni)
- Increase in vaginal pH 4.5
Risk factors
- coexisting infections e.g HIV, chlamydia trachomatis, neisseria
gonorrhoea
- Recent unprotected vaginal intercourse
- Vaginal douching
- Premature rupture of membranes + preterm labour
Lab diagnosis
- pH >4.5
- Whi test (amine test): vaginal uid + 10% KOH -> shy odour
(volatile amines)
Microscopy
- saline mount of vaginal discharge
- Clue cells: squamous epithelial cells with coccobacillary
organisms
- Leucocytes absent
- Gray lm
- Normal vagina ora of lactobacilli replaced by G vaginalis and
others

Mucopurulent cervicitis (MPC)

- in ammation of columnar epithelium of endocervix
Causative agents
- chlamydia trachomatis (most common)
- Neisseria gonorrhoea
- Mycoplasma genitalium
Clinical diagnosis (Cardinal signs)
- yellow mucopurulent discharge from cervix
- Endocervical bleeding upon gentle swabbing
- Edematous cervical ectopic
*signs 2 and 3 more typical of chlamydial infection
*HHV cervicitis produces ulcerative lesions of ectocervix
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 Pelvic in ammatory disease
- polymicrobial infection of upper genital tract (uterus, fallopian tubes, ovaries) -> lead to
infertility, ectopic pregnancy, chronic pelvic pain if untreated
Types
- Primary PID: occurs spontaneously, sexually transmitted
- Secondary PID: occurs after invasive intrauterine procedures (e.g IUD insertion, abortion)
Causative agents
- N gonorrhoea + C trachomatis together with enteric gram negative rods and anaerobes
Pathogenesis
- STI a ecting cervix can initiate process -> permit anaerobic bacteria of vagina to ascend
Risk factors
- sexually active adolescents + young women
Rare causes of PID include:
- Genital mycoplasmas such as M. genitalium,
- Anaerobic (Peptostreptococci) and facultative organisms (Prevotella species)
- E. coli, Haemophilus in uenzae, and group B streptococci
- Secondary to hematogenous dissemination (e.g. tuberculosis or Staphylococcal bacteremia).
Other infections
Bartholinitis - bartholins gland abscess result from infection of bartholin gland +
blockage of its duct
- Anaerobic and polymicrobial infection originating from normal
genital ora are more common
- But can also be caused by N gonorrhoea + C trachomatis
Endometritis

Salpingitis In ammation of fallopian tube

Oophoritis In ammation of ovaries

- extension to peritoneum can cause peritonitis, peri hepatitis,
perisplenitis, pelvic abscess

Fitz-hugh-curtis syndrome - Special form of peri hepatitis, secondary to gonococcal or

chlamydial infection
Clinical features
- right upper quadrant pain
- Edema + erythema of liver capsule
- Exudate with violin string adhesions between liver and peritoneum
Later sequelae
- infertility (if tubes get occluded)
- Ectopic pregnancy (if tubal scarring occurs without occlusion)
- Chronic pelvic pain and recurrent salpingitis
Infections after gynecologic - post operative infections e.g pelvic cellulitis or abscess common
surgery following gynecologic surgery (e.g vaginal hysterectomy)
- Common pathogens: normal vagina ora organisms e.g
anaerobes (peptostreptococci), genital mycoplasmas, aerobic
gram positive cocci and gram negative bacilli

Natal (during birth) infection Bacteria: Group B streptococci, E. coli, Listeria

monocytogenes, N. gonorrhoeae, C. trachomatis
Viruses: CMV, HHV, enteroviruses, hepatitis B virus, HIV.

Genital tract infections in males

Prostatitis (in ammation of prostate gland)
Acute bacterial prostatitis
- caused by N gonorrhoea + C Trachomatis <35 years
- Males >35 common agents are: enterobacteriaeceae + enterococcus
Chronic prostatitis
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 - caused by agents of lower UTI e.g enterobacteriaceae (80%) + enterococcus (15%)
occasionally by pseudomonas
Epididymitis
- young men : mainly C trachomatis, less common by N gonnorhoeae
- Associated with urethritis
- Older men: may be seen following urinary tract instrumentation and usually caused by urinary
pathogens
- In Homosexuals: caused by enterobacteriacae, usually have bacteriuria but no urethritis
Orchitis (in ammation of testicles)
- uncommon + generally acquired by blood borne dissemination of viruses
- Mumps is main agent
- Testicular pain + swelling following infections that range from mild to severe
- Mumps orchitis usually unilateral -> infertility following mumps orchitis is rare

L28 - Rape trauma syndrome

Diagnosis of virginity
Suggestive signs
- intact posterior commissure + fourchette (membranous fold connecting posterior ends of labia
minora)
- Firm rounded labia majora completely closing vaginal or ce which remains closed in lithotomy
position
- Vagina narrow with mucosal rugae
- Firm hemispherical breasts with small nipples surrounded by rosy areolae
Sure signs
- intact hymen 1mm membranous diaphragm partially closing vaginal introits
Hymen
- thin membrane surrounding opening of vagina
- Most common: half moon
Clinical examination of hymen
- done in day light
- Lithotomy potion after doing gentle traction on labia to stretch hymen
- If hymen in tact: should be de ned
- If hymen de orated, must clarify:
• Number of tears/ruptures (single or multiple)
• Position of tears
• Age of tears (recent or old)
• Type of rupture (tears, laceration, remnants)
• Cause of rupture
Variety of hymen
1. Semilunar (crescentic)
- ant or post ori ce
- Most common
- Rupture on both sides
2. Annular
- central ori ce
- Common
- Rupture posteriorly (at 6 o clock)
- May be eshy, elastic and dilatable allowing intercourse without being ruptures
- Elastic hymen ruptures only on rst vaginal delivery
3. Dentate
- ori ce has indentations or folds along its edges, may simulate ruptured hymen
4. Fimbriate
- ori ce has mbria along edges, may simulate ruptured hymen
5. Cribiform
- multiple openings (sieve like appearance)
6. Septate
- opening has septum (longitudinal + transverse) dividing into 2 compartments
- Septum ruptures on rst intercourse
7. Imperforate (no opening)
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- retention of menstrual blood in vagina, tubes and uterus -> hematocolpus + hematometrium
- Condition may simulate pregnancy, resolves through surgical interference by cruciate incision in
center of hymen not reaching circumference
Conditions of valid consent
1. Capacity of giving consent, female should be:
- 16-18
- Not mentally de ciency
- Not weak
- Conscious
• Not under narcosis by drugs e.g date rape drugs such as ketamine, rophynol or gamma-
hydroxy-butric acid (GABA)
• Not under anaesthesia (some females under light anaesthesia may experience sexual
hallucination and charge surgeon for rape, so should be chaperone)
2. Not under violence (moral or physical) as fear of threats as this is considered submission and
prior to act
3. No under fraud
- impersonation of husband during sleep
- Fraudulent therapy by doctors or quacks
Medical examination of rape
Role of physician in examining rape case
- provide immediate medical care, primary level counselling and referral to physical and
psychological sequelae of assault
- Obtain evidence of crime and help judges understand physical and mental condition of woman
and identity assailant
- Write complete report
Procedure
- don't change clothes or bathe before medical exam
- Shouldn’t be examined without authority of investigating magistrate
- Consent of victim/guardian, date/time
- Examine without delay - vulva tenderness, detection of spermatozoa
Statement of victim/history taking
- date and time of alleged o ence
- Details of struggle, resistance
- Pain, haemorrhages, penetration
Preliminary steps in examination
Doctor must record
- person who brought the survivor
- Menstrual + sexual history + infections + pregnancies
- Survivors general behaviour + mental state
- To know if she has had bath/change of clothes
General exam
- conduct + behaviour assessed
- Age (below 7 - max punishment, below 18 - non valid consent)
- Physical development + body build assessed
- Undress victim while standing on clean white sheet to catch any hairs, bres or foreign bodies
falling from clothes
- Sign of general violence resistance or struggle
• Clothes: tears, lost buttons, stains
• Head hair: disarrangement, broken hairs, stains
• Finger nails: broken nails, stains, tag of epithelium under nail bed
• Body: abrasions and bruises, age coincide with date of assault and detected in following sites
- Face and around mouth (petechiae on face - partial asphyxia due to forcible restraint(
- Neck and breast (love bites)
- Arms and legs to prevent her from escaping + abort her resistance
- Inner aspect of thighs to separate them
Genital exam
1. Position of examination
- children and prepubertal: knee chest and supine frog leg position
- Pubertal and adult: lithotomy position
2. Signs of local violence
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 - vulva: tenderness, bleeding; abrasions and bruises
- Pubic hair: matted with semen or blood stains, comb pubic hair for non matching hair, root
study
- Loose hair of assailant may be found
- Hymen: recent or old tears may be found
- Apply toluidine blue dye then rinse with vinegar to visualise hidden or minor injuries. Dye is
taken up by metabolically active cells
• Dried seminal stains on the external genitals and thighs are scraped o by means of a clean
blunt knife for subsequent examination.
• Vaginal secretion obtained by introducing a sterile cotton wool swab for presence or
spermatozoa within 24 hrs (Slide test). Any muco-purulent/ purulent discharge is examined
for signs of STD.

Rape on a virgin Rape of de orate women Rape on children

- laceration + rupture of hymen - even without childbirth hymen - no signs of general violence
- Tearing posteriorly at sides or destroyed vaginal ori ce (child has no understanding)
in middle dilated mucous membrane - Minimal signs in young children
- Margins sharp and bleed on thickened and wrinkled (due to deep hymen and
touch - Local signs minimal or even narrow vagina) -> di cult/
- Labia minora swollen + tender absent only evidence is semen impossible penetration
- Scratches and bruises by - Resistance - local injury, - If brutal force applied, severe
ngers of assailant which will tearing of vagina perineal tears and laceration
be dark red, purple in 24 hours, - Older women - senile atrophy occurs
vagina and cervix and friability - extensive vaginal - During penetration penis
- 3-4 days edges of laceration lacerations and perineal trauma compresses labia, causing
congested and swollen, heal in - Injuries obscure in 3-4 days bruises
1 week and never unite - Tears: hymen posterior, ant and
post vaginal wall, perineum,
anterior anorectal canal,
vaginal herniation of abdominal
viscera
Specimens to be collected from victims
- avulsed head hairs + pubic hair
- Pubic hair combings
- Blood group, pregnancy test, hep B and AIDS, venereal diseases as chlamydia, syphyillis or
gonorrhoea
- Urine drug screening
• Rohypnol (Flunitrazepam) - found in urine up to 36-72 hours
• GHB (Gamma hydroxybutyric acid) - found in urine up to 12 hours
• GBL (gamma butyrolactone) - found in urine up to 12 hours and in blood up to 6 hours
• Nails scrapings for blood or tissue
• Saliva for secretor group
• Swabs from bite marks or saliva
Examination of accused
a) The consent for examination is mandatory. It should be written & witnessed even if he is
imprisoned.
b) His own story has to be compared with the victim's one & other stories given before.
c) His age if less than 14 years; he is considered by law incapable of committing the crime of
rape.
d) Sexual power (Potency) should be assessed as impotency may be alleged by the accused as a
defense.
e)Specimens collected: Pubic hair combings, Avulsed pubic hair, Head hair, Blood group, Nail
scrapings for blood or tissue, Swabs from coronal sulcus, prepuce, urethra
Sequelae of rape
Death due to
- shock due to emotion/blunt force
- Haemorrhage from genitalia/peritoneum
- Su ocation/strangulation
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 Psychological trauma - mental derangements, convulsions epilepsy
Rape trauma syndrome - disrupt patients physical social and sexual life
Rape trauma syndrome
- psychological trauma experienced by a rape victim that includes disruptions to normal physical,
emotional, cognitive, interpersonal behaviour
1) Acute phase - feelings of shock, disbelief and helplessness
- Concern about pregnancy, sexual transmitted infections or injury
- Inability to concentrate
- Some victims may seem completely in control like nothing happened
Can be classi ed as one of three responses
- expressed: survivor may appear agitated or hysterical and may su er from
crying spells or anxiety attacks
- Controlled: ne and without emotions
- Shock/disbelief: strong sense of disorientation
2) Repression phase - avoids thinking and talking about the assault
- Experiences anger
- Tells others he/she is over it
- Minimises assault

3) Reorganisation phase - Hyper vigilance

- Depression
- Flashbacks and nightmares
- Lack of trust
- Fear and avoidance of people and places that remind him/her of assault

4) Integration phase - regains feelings of control and safety

- Shifts blame from self to perpetrator
- Regains trust in others
What happens if a victim does not report
- no investigation, prosecution, record of assault other than anonymous evidence if victim
chooses
Victims who le a report
- allows law enforcement to start investigating
- Protects victim and their community
- Even if victim is unsure about prosecuting, the report enables the police to investigate while
evidence is fresh
- If victim doesn't choose to prosecute, evidence can be helpful if they assault another person
Once report has been led
Victim has three options
1. Criminal charges against rapist
2. Civil charges against rapist
3. Charges against a third part
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L29 - Drug therapy of STDS
Syphilis (Treponema pallidum - spirochete bacterium)
Primary syphilis - genital ulcer/sores, rm round painless
Secondary syphilis - skin and mucosal lesion
Latent syphilis - serologically positive but asymptomatic (1-2 years)
Tertiary syphilis - neurosyphilis, CVS or gummatous syphilis (4-5 years)
Gold standard for Penicillin G
syphilis 1) Parenteral benzathine penicillin G (for all stages)
- Early treatment, Single IM dose (Long acting)
- Late syphilis: 3 doses at weekly intervals
2) Aqueous crystalline penicillin (IV, short acting)
- used for neurosyphilis, ocular syphilis, congenital syphilis
- High CNS penetration, short half life, requires frequent dosing
3) Procaine penicillin G (IM, intermediate action)
- 12-24 hours, daily for 14 days + probenecid (increase penicillin
availability in CSF)
- Supplemented by a 3 day course of prednisolone
- Use: neurosyphilis (alternative)
- Increase CSF penicillin concentration
Others Doxycycline
- oral
- For non pregnant patients allergic to penicillin
Erythromycin
- oral
- For pregnant patients allergic to penicillin + penicillin for baby at birth
(erythromycin crosses placenta poorly)
Treatment of syphilis in pregnancy
- penicillin drug of choice (second dose of benzathine penicillin G, 2.4 million units IM
administered a week after initial dose to prevent congenital syphilis)

In case of penicillin hypersensitivity

- penicillin desensitisation (Best option)
- Alternatives
• Treatment with erythromycin (crosses placenta poorly -> wont protect fetus so newborn still
much receive penicillin at birth)
• Intramuscular ceftriaxone, 500mg daily for 10 days (no su cient evidence)

Important risk in pregnancy

- women treated in second half at pregnancy are at risk of premature labour or fetal distress if the
treatment precipitates jarisch-herxheimer reaction

Jarisch-Herxheimer reaction
- acute febrile reaction that follows antibiotic treatment
- Headache, malaise, myalgia (resolves in 24 hours)
- Worsening of neurological ophthalmic disease, myocardialischemia and laryngeal stenosis
might occur
- Fetal distress/premature labour occur in pregnancy
- Prednisolone 40-60mg daily for 3 days (prevent reactioN)
- Antibiotics can be started 24 hours after steroids
- In high risk patients (pregnant women, neurosyphilis, ocular syphilis) rst antibiotic dose
should be given in hospital under monitoring
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 Gonorrhoea (Gram negative diplococcus, Neisseria gonorrhoea)
Uncomplicated gonorrhoea
- First line: Ceftriaxone 1g IM as single dose (3rd generation cephalosporin)
- Alternative: cipro oaxin 500mg orally as single dose (Fluoroquinolone)
Pregnancy + breastfeeding
- First line: ceftriaxone 1g IM (safe in pregnancy)
- Alternative: spectinomycin 2g IM stat
Disseminated gonorrhoea (systemic infection: arthritis, endocarditis, meningitis)
- ceftriaxone 1g IM or IV daily or Cefotaxime 1g IV 3 times daily
Switched to an oral alternative according to sensitivities after 48 hours and continued for 7 days

Chlamydia (Gram negative chlamydia trachomatis)

Uncomplicated
- rst line: doxycycline 100mg orally twice daily for 7 days
- Alternative: azithromycin 1g orally single dose -> followed by 500mg daily x2 days
Complicated cases (e.g epididymo-orchitis
- rst line: doxycycline 100mg orally twice daily for 14 days
- Alternative: o oxacin 400mg orally 2x daily for 14 days

Chancroid (Haemophilus ducryei)

- Azithromycin (1 single oral dose) or Ceftriaxone IM (single dose)
- Alternatives: cirpo oaxin, erythromycin
Granuloma inguinale (klebsiella gramulomatis)
- azithromycin unti leisions heal
- Alternative: doxycycline, cipro oaxin, erythromycin
Urethritis
Causative organisms
Gonococcal urethritis Non-gonococcal urethritis

- Neisseria gonorrhoeae - Chlamydia trachomatis

- Trichomonas vaginalis
- Mycoplasma genitalium
- Herpes simplex virus / Adenovirus
- Ureaplasma urealyticum
- Neisseria meningitidis
Treatment
Ceftriaxone
- 500mg Im once (for persons <150kg)
- For neisseria gonorrhoea/meningitides
Doxycycline
- 100mg orally 2x daily for 7 days
- All urethritis
Alternatives
- azithromycin 1g orally (if doxycycline not suitable
- Metronidazole/tinidazole 2g orally once (if trichomonas vaginalis con rmed by microscopy,
culture, NAAT or when symptoms persist)
Bacterial vaginosis
- anaerobic organism
Metronidazole orally 500mg 2 times per day for 7 days

Trichomoniasis (Trichomonas vaginalis)

Metronidazole
- men: 2g orally single dose
- Women: 500mg 2 times for 7 days
Or
Tinidazole 2g orally single dose
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 Vulvovaginal candidiasis (candida albicans)
Over the counter agents
- clotrimazole 1% cream 5g intravaginally for 7-14days/2% for 3 days
- Miconazole 2 % cream 5g intravaginally for 7 days/4% daily for 4 days
Oral agent
- uconazole 150mg orally in single dose

HIV (Anti-retroviral therapy/ART)

Pregnancy does NOT contraindicate ART.
Drugs safe in pregnancy:
• Zidovudine
• Lamivudine
• Nevirapine
• Nel navir
• Saquinavir
First-line regimen (pregnant women, National AIDS control):
• Zidovudine + Lamivudine + Nevirapine
Risk of transmission (mother -> neonate)
- without ART: 30% risk
- With ART: <2%
Chemoprophylaxis
Gonorrhoea + syphilis
- procaine penicillin 2.5MU I.M + probenecid 1g orally
- Allergic patients: doxycycline 100mg BD x 15 days
Chancroid, lymphogranuloma venereum, granuloma inguinale
- doxycycline 100mg BD X 15 days
Infective disorders of male genital tract
Prostatitis Acute
- Initial: parenteral treatment with uoroquinolone (broad spectrum)/ b lactam
with amino glycoside
- After: switch to oral regimen according to susceptibility testing
- Ampicillin 1 g every 6 hours -> Gentamicin every 8 hours -> cipro oaxin
4-6 weeks
Chronic
- Cotrimoxazole (trimethoprim + sulfamethoxazole): penetrates well into acid
prostatic secretion
Or
- Cipro oaxin for 4-12 weeks (achieve good concentration in prostate)
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 Balanoposthitis Fungal infections (Candida, Gardnerella)
(in ammation of - anti fungal creams (Nystatin or Clotrimazole) locally over applied clean dry skin
glans and - Oral anti-fungal drus (e.g uconazole)
foreskin) - Circumcision
Bacterial infection
- 1st gen oral cephalosporin e.g cephalexin/cefadroxil

Genital herpes HSV-2

- acyclovir/valacyclovir orally for 7-10 days
- If symptoms dont resolve in 3-4 days consider secondary infection/wrong
diagnosis
- If lesion persist for more than 14 days re ect HIV co-infection

L30 - Prevention and control of STI’s and STD’s

Sexually transmitted diseases
Health impact of STI’s
- Stigmatisation
- Infertility
- Cancers
- Pregnancy complications
- Increase HIV risk
Drug resistance
- major challenge in STI control
- Especially concerning for gonorrhoea
Consequences of STDs beyond immediate infection
1. Increased HIV risk
- STIs raise acquisition risk 2-3 fold
- Especially linked to: HSV type 2, gonorrhoea, syphilis
2. Reproductive health consequences
- Infertility
- Adverse pregnancy outcomes
- Mother-to-child transmission risk
- Gonorrhoea & chlamydia -> major cause of PID -> infertility in women
3. Mother to child transmission
- possible outcomes:
- Stillbirth
- Neonatal death
- Low birth weight and prematurity
- Sepsis
- Neonatal conjunctivitis
- Congenital deformities
4. Cancer risk
- HPV cause cervical can cancer
- Hep B : cause death from cirrhosis + hepatocellular carcinoma
Epidemiology of STD
Major pathogens
- 4 curable: syphilis, gonorrhoea, chlamydia, trichomoniasis
- 4 incurable: hep B, HSV (herpes simplex), HIV, HPV
• Symptoms can be reduced/modi ed but not cured
• Vaccines available for Hep B and HPV
Transmission
- Sexual contact: vaginal, anal and oral sex
- Non sexual transmission
• Blood / blood products
• Mother-to-child (vertical transmission):
• Infections: Chlamydia, Gonorrhea, Hepatitis B, HIV, Syphilis
• During pregnancy → HIV, Syphilis
• At delivery → Gonorrhea, Chlamydia, HIV
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 • After birth → HIV
• Through breast milk → HIV
• Needle sharing / injections
• Unsterilized needles, injections (e.g., Syphilis, HIV, Hepatitis B).
• Tissue transfer
• From infected persons.
- Host: human
Age
• Peak incidence: 15–24 years.
• Highest incidence: sexually active adolescents.
• Risk is higher in 15–19 years and 20–24 years due to:
◦ Behavioral factors (risk-taking behaviors).
◦ Biological factors (immature immune system, cervical ectopy).
◦ Cultural factors (norms, stigma, access issues).
• Young females:
◦ More susceptible due to cervical ectopy (columnar cells at the cervical canal
surface → more prone to infections compared to strati ed squamous epithelium).
Gender
• STIs are more reported in females.
Racial Factors
• Higher rates in some racial/ethnic minorities vs. whites.
• Linked to social conditions: poverty, lower education, fewer job opportunities.
Socioeconomic Factors
• More common in lower socioeconomic groups.
Education Level
• Higher incidence among those with lower education levels.
Cost of Treatment
• Major burden on healthcare systems.
• Example: $16 billion/year in the US

Social Factors Facilitating Spread of STIs

• Prostitution & commercial sex work → high transmission risk.
• Broken homes → unstable family environments increase vulnerability.
• Sexual disharmony (strained relationships, divorce, separation).
• Economic factors → poverty in developing countries promotes risk.
• Emotional immaturity → impulsive/risky sexual behavior.
• Urbanization & industrialization → isolation from family, increased mobility.
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 • International travel → rapid global spread of resistant strains (e.g., N. gonorrhoeae, HIV/
AIDS).
• Changing behavioral patterns → relaxation of moral/cultural values.
• Social stigma → delayed detection, non-disclosure of contacts, treatment dropout, self-
treatment.
• Alcoholism (indirect e ect) → increases risky behaviors, prostitution; prostitution may in
turn fuel alcohol sales.
• Inadequate sex education & poor health information.
• Delayed marriage → prolonged period of premarital sexual exposure.

STI control
Goal: Reduce incidence and prevalence through multi-pronged strategies.
Five main areas:
1. Epidemiologic targeting → identify priority groups and regions.
2. Reliable data → support decision-making.
3. Primary prevention & access → condoms, vaccines, health promotion.
4. Enabling environment → supportive laws, stigma reduction, education.
5. E ective clinical services → shorten infectivity period, ensure treatment access.
Clinical Presentations of STIs
General Features
• Many STIs: asymptomatic or mild symptoms → often unrecognized.
• Symptoms can be non-speci c.
• Underreporting due to:
◦ Lack of symptoms.
◦ Stigma.
Most Common Symptoms
• Vaginal discharge.
• Urethral discharge / burning in men.
• Genital ulcers.
• Abdominal pain.
Diagnosis
• High-income countries:
◦ Use molecular diagnostic tests → accurate, detect asymptomatic infections.
• Low-/middle-income countries:
◦ Limited access to molecular tests.
◦ Expensive, slow results → delayed follow-up, incomplete care/treatment.
Prevention and control of STI’s
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 Algorithm for HIV Post-Exposure Prophylaxis (nPEP)
Substantial Risk for HIV Acquisition
• Exposure: vagina, rectum, eye, mouth, or mucous membrane;
percutaneous contact.
• With: blood, semen, vaginal/rectal secretions, breast milk, uids
contaminated with blood.
• When: Source known HIV-positive → nPEP recommended.
• Source unknown HIV status → Case-by-case decision.
Negligible Risk for HIV Acquisition
• Exposure: urine, nasal secretions, saliva, sweat, tears (if no blood).
• Regardless of source’s HIV status → nPEP not recommended.
Timing
• ≤72 hrs post-exposure → Consider nPEP.
• >73 hrs post-exposure → nPEP not recommended.
Secondary 1. Awareness & Health-Seeking
prevention • Promote disease awareness → improves recognition of STI symptoms →
increases care-seeking.
• Promote early healthcare-seeking & reduce stigma.
2. Case Management
• Ensure accessible, acceptable, and e ective case management via public
& private healthcare.
• Syndromic diagnosis algorithms useful at primary care level.
3. Diagnostic Tests
• Promote accurate diagnostic tests (esp. molecular).
• Rapid tests (syphilis, hepatitis B, HIV) → inexpensive, minimal training,
results in 15–20 mins.
• Examples: rapid syphilis & dual HIV/syphilis tests (used in resource-limited
settings).
4. Access & Screening Services
• Remove barriers to care (a ordability, accessibility).
• Screening integrated into:
◦ Maternal care, premarital screening.
◦ Blood/tissue/semen donation.
◦ Occupational health schemes.
◦ Sex worker programs.
◦ Primary healthcare.
5. System Strengthening
• Integrate STD services into general healthcare (e ective referral system).
• Provide treatment guidelines and access to e ective drugs.
• Train healthcare providers → diagnosis of syndromes (e.g., discharge,
ulcers, abdominal pain).
• Ensure partner noti cation & treatment.
• Support patient adherence to drugs.
6. Victim Support & Con dentiality
• Provide services for victims of rape/sexual abuse → exam, counseling,
treatment, specimen collection (for legal readiness).
• Educate patients on reducing transmission risks.
• Expedited Partner Therapy (EPT / PDPT): partners treated via patient-
delivered medication without clinical visit.
• Ensure reporting & con dentiality (protected by law/regulation).
7. Targeted Interventions
• Epidemiologic targeting & presumptive treatment → focus on “hot spots”
(e.g., sex workers).
• Reducing STI prevalence blunts HIV transmission (cofactor e ect).
◦ Ulcerative STIs (chancroid, HSV-2, syphilis) = major HIV cofactors.
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 Treatment & Screening (CDC Recommendations)
Bacterial Vaginosis (BV)
• Most common cause of abnormal vaginal discharge.
• Symptoms: shy odor, abnormal discharge.
• Tx: Metronidazole or Clindamycin (oral/vaginal).
• Asymptomatic cases → controversial, but recommended in pregnant
women with prior preterm births.
Screening Guidelines
Chlamydia & Gonorrhea
• Sexually active women <25 yrs.
• Pregnant women <25, and older women if at risk.
• Homosexual men: annually or q3–6 months if high risk.
• Persons with HIV: at diagnosis, then annually.
Syphilis
• Asymptomatic adults at increased risk.
• All pregnant women → rst prenatal visit, repeat at 28 wks & delivery if high
risk.
• Homosexual men: annually or q3–6 months if high risk.
• Persons with HIV: at diagnosis, then annually.
Herpes (HSV)
• Consider type-speci c serology for women with suspected STI.
• Routine HSV-2 screening not recommended for asymptomatic pregnant
women.
• Homosexual men: type-speci c serology if symptomatic or at risk.
Trichomonas
• Screen women at high risk.
• Persons with HIV: at diagnosis, then annually.
HIV
• All women evaluated for STIs.
• Pregnant women: screen at rst visit; repeat in 3rd trimester if high risk.
• Homosexual men: annually; more frequent if multiple partners.
Hepatitis B
• Women at risk.
• All pregnant women → HBsAg at rst prenatal visit (regardless of history).
• Homosexual men → screened for HBsAg, anti-HBc, anti-HBs.
Tertiary • Follow-up of cases
• Education and counseling to reduce/prevent future risk-taking behavior;
• Monitor and respond to STI antimicrobial resistance
• Ensure the availability of an e ective surveillance system
• Monitor and evaluate the e ectiveness of the STDs control program
• Ensuring the sustainability of improved STDs services
• Provision of counseling and long-term psychological supports for victims
of rape & children sexual abuse
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