Stis

Front 1

Main Bacterial STIs

Back 1

Front 2

NON-Bacterial STIs

Back 2

Front 3

The major viral STIs

Back 3

HIV
Genital Herpes – HSV types 1 and 2
Genital warts – HPV types 6 and 11
Genital dysplasia and cancer – HPV types 16 and 18 and others
Hepatitis B - HBV

Front 4

The major bacterial STIs

Back 4

Gonorrhoea Neisseria gonorrhoeae
Chlamydia Chlamydia trachomatis
Syphilis Treponema pallidum
Mycoplasmas and Ureaplasmas
Tropical infections (chancroid, LGV and Donovanosis)

Front 5

Other important STIs or conditions associated with sexual activity

Back 5

Trichomoniasis – Trichomonas vaginalis
Bacterial vaginosis

Front 6

Early Events in Trans-mucosal
HIV-1 Infection.

Back 6

The arrows indicate the path of the virus.
The viral-envelope protein binds to the
CD4 molecule on dendritic cells.
Entry into the cells requires the
presence of CCR5, a surface chemokine
receptor.
Dendritic cells, which express
the viral co-receptors CD4 and CCR5,
are selectively infected by R5
(macrophage-tropic) strains.
Within two days after mucosal exposure,
virus can be detected in lymph nodes.
Within another three days, it can be
cultured from plasma.

Front 7

HPV Immunisations

Back 7

70% of Ca Cervix are caused by 16, 18
90% of Genital warts are caused by 6, 11
Gardasil: immunity to 6, 11, 16, 18
Cervarix: immunity to 16, 18

Front 8

HPV infection

Back 8

Front 9

Dynamic relationship between HPV infection & Cervical health

Back 9

Originally thought there was inevitable progression from low grade abnormalities to high-grade abnormalities to cervical cancer

Now recognised that LSIL cytology is a manifestation of acute HPV infection, and that most LSIL regresses over time

The absolute risk of cancer associated with a high-grade abnormality difficult to determine from available observational data, but is estimated at < 1% per year

Front 10

Pap smear

Back 10

Most patients with a Pap-smear report of HGSIL have CIN II or III, but some have invasive disease. Thus, the Pap smear is only a screening test, and a biopsy is required for a definitive diagnosis.

Front 11

Back 11

Panel A
shows the colposcopic appearance of the
cervix in a patient with a Pap-smear report
of HGSIL. The lesion surrounding the
cervical os is barely visible.

Panel B
shows the same lesion after the
application of a dilute solution of acetic
acid, which highlights areas high in
nucleic acid. Subsequent biopsy of
this lesion revealed CIN III.

Front 12

Cancer & HPV infection

Back 12

Increased risk in of anal cancer in men who have sex with men and higher if HIV positive people
Oncogenic HPV cause vulval and vaginal cancers – HPV found in 75-90%
HPV is also implicated in 25% of head and neck cancers – mainly of the oropharynx

Front 13

Genital WartsRegression & Recurrence

Back 13

If left untreated, 20% of patients spontaneously regress within 6 months

1 in 3 patients experience recurrence after successful treatment

Front 14

HSV

Back 14

Herptic lesion on the buttock (genetia herpies)
Public toilet (atypical locations)
Stay with the DRG fro the rest of the life

Can be infectious even with lack of symptoms

Front 15

Neisseria gonorrhoeae on cells of fallopian tube

Back 15

Front 16

N. Gonorrhoeae Clinically

Back 16

Adherence, Pinocytosis
Inhibition of ciliary function
Destruction of tissue
Inflammation
Purulent exudate in lumen of infected organ
Incubation 1 - 14 d (av. 7 days in male)
Risk of acquisition from an infected contact
20% for males from females
50% for females from males

Front 17

Gonorrhoea urethral exudate - Gram Stain

Back 17

Male urethera discharge
- diplococci

looks similar to emningococci gram stain but M.C is plumper

Front 18

Neisseria gonorrhoeae (Ng)Survival

Back 18

Ng grows in endocervix
Ng requires nutrient enriched media for
growth e.g., “chocolate” agar
Ng do not tolerate drying
Ng do not have a true capsule
Ng have an absolute requirement for iron
e.g., serum glycoprotein transferrin
Ng are bacteria of human beings

CANT CATCH IT OFF A TOILET SEAT

Front 19

Neisseria gonorrhoeae (Ng) Spread and Multiplication

Back 19

On mucosal cell surface the Ng multiply rapidly

Ng spread upwards in the urethra in the male and through the cervix in the female

Ng stick to spermatozoa and hitch a ride

Front 20

Toll-like
Receptor 4
(TLR4)

Back 20

Front 21

COMPLEMENT

Back 21

Front 22

Gonococcal infection in females is different to infection in males

Back 22

Within minutes of infection of primary cervical epithelial cells, complement protein C3b is deposited on the lipid A portion of gonococcal lipo-oligosaccharide (LPS) and is rapidly inactivated to iC3b.

Ng inactivates C3b, stopping inflammation in the lower genital tract of females, 50-80% of whom are asymptomatic.

Approximately 45% of women with gonococcal cervicitis will develop an ascending infection, the prerequisite to PID.

CR3 progressively decreases in an ascending manner from the ectocervix to the fallopian tubes

70 to 90% of women with disseminated infection lack signs of genital tract involvement

Front 23

Gonococcal Adaptation

Back 23

Gonococci have adapted multiple mechanisms by which they can evade the lytic action of the complement system including:
C4b inactivation &
Formation of a non-functional Membrane Attack Complex (MAC) on their cell surface

Front 24

Hyperacute Gonococcal Conjunctivitis

Back 24

Front 25

Chlamydia Characteristics

Back 25

Family Chlamydiaceae
Small obligate intracellular bacteria
Gram-negative
Range in size from 0.2 to 1.5µm in diameter
There are 18 serovars of C. trachomatis

Front 26

Chlamydia Lifecycle

Back 26

1. The Elementary Body (EB)
Small 0.3µm in diameter
Round, tough spore like structures allowing survival outside of the host
Rigid cell wall
Infectious form of the organism
Non-replicative

2. The Reticulate Body (RB)
Larger in size – 1µm
Represent the replicating stage of the cycle
Synthesise DNA, RNA and proteins
Non –infectious form of the organism

Front 27

Chlamydia trachomatis
- and ATP

Back 27

Unique growth cycle

Depends on host cell to supply ATP and essential nutrients

Lacks system for electron transport

No cytochromes

Cannot synthesise ATP

Front 28

Notification of Chlamydial Infections (NSW)

Back 28

Primarily a disease of men and women 15-35

Front 29

Chlamydia trachomatis
Pathogenesis

Back 29

No latency

Elevated antibody titre

Disease due in part to hypersensitivity (worse if had previous infection)

Self-limiting to low-grade persistent infection for years; re-activation

Front 30

Ovarian tube defects

Back 30

Front 31

Chlamydia trachomatis
Immunity

Back 31

Not protective

Ct do not survive well in PMNL’s

Vaccine not yet developed

g - interferon can inhibit

Front 32

Chlamydia and blindness

Back 32

Inflammation leads to damage and attempts at repair (fibrosis & scarring)

Front 33

Treatment for Chlamydial Infections

Back 33

Azithromycin is the preferred treatment but the down-side is that there is significant resistance in other STI agents (T.pallidum & N.gonorrhoeae) to Azithromycin.
Widespread resistance in N.gonorrhoeae to tetracyclines, but doxycycline has useful activity against syphilis.

Front 34

Mycoplasmataceae

Back 34

Mycoplasmas & Ureaplasmas
First isolated in 1937
Family Mycoplasmataceae
Two genera Mycoplasma and Ureaplasma
Lack cell wall
Smallest free living microorganism both in genome size and cellular dimension (300 nm)

Front 35

Mycoplasmas & Ureaplasmas
Pathogenesis

Back 35

Attach to the cell via a tip structure
Following attachment, the plasma membrane of the host appears to be forced inward, suggesting the organism must enter the cell by receptor-mediated endocytosis
Ureaplasmas differ from Mycoplasmas – have enzyme urease

Front 36

Treponema pallidum (Tp)

- staining

Back 36

Does not stain by Gram’s method.
Not yet cultured in vitro.
Not visible by light microscopy except by ‘dark-field’ or fluorescence microscopy
A “silver stain” thickens the spirochaete to be seen in specimens examined by light microscopy
Surface rich in lipid, Tp evades host response

Front 37

Treponema pallidum (Tp)Infection

Back 37

Incubation period related to initial inoculum size :
107 organisms; lesion 5-7 days
50-100 organisms; lesion 3 weeks

Spirochaete attaches by end

Tp has neither LPS nor toxin

Tp chemotaxic

Front 38

Syphilis (T. pallidum)Primary stage - chancre

Back 38

Multiplication of Tp at site of infection
Patient highly infectious
Associated host-antibody response:
specific anti-Tp; IgM and IgG
non-specific non-Tp (anti-cardiolipin); Veneral Disease Research Lab. (VDRL) test positive (2/3), now EIA, may take 3 mth to +ve
Chancre infiltrated with lymphocytes and macrophages

Front 39

Dark Ground Microscopy

Back 39

Standard bright field light microscopy light is shone onto the specimen yielding a bright background
Dark field microscopy the condenser excludes direct light allowing scattered light to focus on the specimen
Bacteria appear luminous against a dark background
Helical rods with Corkscrew motility 0.18microns
x 6-20 microns long

Front 40

Syphilis (T. pallidum)Secondary stage

Back 40

3-6 weeks after chancre when local response brings primary stage under control
Systemic infection
Haematogenous spread through body
Lesions in skin (where temp is less)
Systemic immune response
Persists for weeks or months

High anti-Tp titres (no DTH)

“Premunition”
resists challenge
unable to clear existing lesion

Infection persists
Formation of immune complexes
Immune complexes deposited in kidneys, joints etc (Type III Hypersensitivity)
Host response suppresses lesions giving “latent” period, but infection not controlled
DTH uniformly positive
Tp persists in spite of antibody

Front 41

Secondary Syphilis

Back 41

Not itchy
Any rash especially if not itchy should include syphilis in the differential diagnosis
- Classically on the palms and sole

Front 42

Premunition

Back 42

able to resist challenge from re-infection but unable to clear the exisitng lesion

Front 43

Syphilis (T. pallidum)Tertiary stage:

Back 43

1 - 20 years after primary stage

Gummas (granulomatous lesions) in soft tissue
Neurological involvement
Syphilis & HIV

Front 44

Back 44

Granulomatous response fails to kill pathogen but causes tissue damage and illness

Front 45

Late syphilis:
Multiple Gummata

Back 45

Front 46

Trichomonas vaginalis

Back 46

Protozoan
Attaches to mucous membrane
Anaerobic
Infects sites covered by squamous but not columnar epithelium
Urethra (male); vagina (female)
No invasion of mucosa
Frothy malodorous discharge
Symptoms: nil to profound acute inflammation

Front 47

Trichomonas vaginalis Morphology

Back 47

Occur in several sites in a number of animals
Commensal in GIT in man, only known human pathogen
Motile protozoan, pear-shaped, ~10x7 μm
Single nucleus, 5 flagella, undulating membrane, characteristic motility
No cyst form recognised
Capable of phagocytosis

Front 48

Vaginal flora

Back 48

Multiple mixed organisms - composition varies with age, menstrual cycle, sexual experience, antimicrobials
Anaerobes predominate and lactobacillus species common - most produce H2O2
Low levels of coliforms and Gardnerella
Staph aureus, haemolytic streptococci in minority

Front 49

Bacterial Vaginosis

Back 49

Mixed microorganisms e.g.
Gardnerella vaginalis (+++)
Prevotella spp., Mobiluncus spp. (+)
Mycoplasma hominis (+)

Malodorous vaginal discharge, adherent to vaginal wall

“clue” cells

Front 50

Normal Vaginal Swab (Gram Stain)

Back 50

Front 51

Bacterial Vaginosis

Back 51

Front 52

Proposed Pathophysiology of Bacterial Vaginosis

Back 52

The overgrowth of anaerobic microorganisms is
accompanied by the production of proteolytic enzymes
that act on vaginal peptides to release several biologic
products, including polyamines, which volatilize in the
accompanying alkaline environment to elaborate
foul-smelling trimethylamine.

Polyamines act to facilitate the transudation of vaginal fluid
and exfoliation of epithelial cells, creating a copious
discharge.

Clue cells are formed when Gardnerella vaginalis, present
in high numbers, adhere in the presence of an elevated
pH to exfoliated epithelial cells.

Front 53

Bacterial Vaginosis – Diagnosis

Back 53

Front 54

Bacterial Vaginosis is an STI

Back 54

Sexual contact – male or female
Increased by multiple contacts
Decreased by condom use
Increased risk if male uncircumcised (cf other STIs)

Front 55

Bacterial Vaginosis – Risk Factors

Back 55

Use of vaginal foreign bodies, perfumed soaps, or douching
Cigarette smoking
Intrauterine device
New male sexual partner
Sex with another woman
No condom use (trend toward association)

Front 56

Significance of Bacterial Vaginosis

Back 56

Nuisance value, associated with obstetric syndromes, increased rate of preterm birth (usually with chorioamnionitis); postoperative wound infections

Possible increased risk of acquiring other STIs including HIV

Front 57

Gardnerella vaginalis

Back 57

Gram-variable rod
Recognised by β haemolysis on blood agar
Susceptible to wide range of antibiotics
Normal habitat human vagina (up to 70% adult women), some girls, rectum
Found in ~100% of women with BV, but causative role not clear
Often in male urethra but no known significance
Adheres to vaginal epithelial cells
May produce cytotoxins

Front 58

Bacterial Vaginosis – Treatment

Back 58

Front 59

Candidiasis

Back 59

A primary or secondary mycotic infection caused by members of the genus Candida. The clinical manifestations may be acute, subacute or chronic to episodic.

Involvement may be localized to the mouth, throat, skin, scalp, vagina, fingers, nails, bronchi, lungs, or the gastrointestinal tract, or become systemic as in septicaemia, endocarditis and meningitis.

Distribution: World-wide.

Aetiological Agents: Candida albicans, C. glabrata, C. tropicalis, C. krusei. C. parapsilosis, C. guilliermondii and C. pseudotropicalis. All are ubiquitous and occur naturally on humans.

Front 60

Back 60

Oral candidiasis in an infant showing characteristic patches of a creamy-white to grey pseudomembrane composed of blastoconidia and pseudohyphae of C. albicans. Note the mouth of normal newborn infants has a low pH which may promote the proliferation of C. albicans. The infections are usually acquired during the birth process from mothers who had vaginal thrush during pregnancy. Clinical symptoms may persist until a balanced oral flora has been established.

Front 61

Vulvo-Vaginal Candidiasis - Treatment

Back 61

Consider other non-STI possibilities
Vaginitis – local or systemic illness
Allergic vaginitis
Atrophic vaginitis
Chemical/irritant vaginitis
Desquamative interstitial vaginitis
Erosive lichen planus vaginitis
Systemic illness
Behçets disease

Front 62

Donovanosis
Calymmatobacterium granulomatis

NOW KNOWN AS:
Klebsiella granulomatis

Back 62

Begins as single or multiple subcutaneous nodules that soon erode through skin
Results in fleshy, beefy-red, exuberant granulation tissue which bleeds readily
Genital erosion
Lesions expand by direct extension and autoinoculation
Haematogenous spread

Front 63

Lymphogranuloma venereum

Back 63

LGV is also caused by Chlamydia trachomatis but:

Not restricted to epithelial surfaces

Is invasive and causes severe inflammation

Preference for lymphatic tissue

Primary stage is asymptomatic small genital ulcer – self-resolving

Then painful lymphadenopathy with systemic illness

Front 64

Genital Ulcers – Non-venereal

Back 64

Front 65

ChancroidHaemophilus ducreyi

Back 65

Gram negative bacillus

Requires X-factor (hemin)

Incubation period 4-7 days

First symptom - ulcer

Front 66

Swab & Urine Specimen Collection - Males

Back 66

Urethral specimens
Do not pass urine for at least 4 hours prior to specimen collection

First catch urine 
Should not pass urine for at least 3 hours before the sample collection
Collect first 10ml of urine
Voiding < 30 minutes prior to collection may influence results

Distal  urethral  swab
Performed when discharge or urethritis symptoms
Confirm a positive urine PCR for gonorrhoea
Test a gonorrhoea contact
Test of cure after treatment for gonorrhoea

Proximal urethral swab 
Performed when chlamydia testing required and urine not taken for chlamydia PCR

Other: Rectal, Pharyngeal, Ulcer/Lesion

Front 67

Swab & Urine Specimen Collection - Females

Back 67

Endocervical specimens
Do not pass urine for at least 4 hours prior to specimen collection

Vaginal specimens
Lateral vaginal wall (Candida, Bacterial Vaginosis)
Posterior fornix (Trichomonas)

First catch urine 
As per males (if endocervical swab not available)

Other: Rectal, Pharyngeal, Ulcer/Lesion

Front 68

Urethral Discharge Steps

Back 68

Front 69

Urethral Discharge Tx

Back 69

Front 70

Presistent/recurrent urtheral discharge in men

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Front 71

Gential Ulcers

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Front 72

Gential Ulcers Tx

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Front 73

Vaginal Discharge

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Front 74

Vaginal discharge:
Speculum

Back 74