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Transcript
Sexually Transmitted
Diseases
Sexually Transmitted
Diseases










Chlamydia trachomatis √
 Genital Chlamydial
Lymphogranuloma
Infection
venerum √
 Gonorrhoea √
Neisseria gonorrhoea √
 HIV infection/Hepatitis
HIV/Hepatitis B √
 Ano-Genital Warts √
Papillomaviruses
 Genital Herpes √
Herpes simplex I , II
 Syphilis √
Treponema pallidium
 Trichomoniasis √
Trichomonas vaginalis
 Chancroid √
Haemophilus ducreyi
 Crabs √
Pediculosis Pubis-Phthirus
pubis
√=notifiable
Granuloma Inguinale √, Candidiasis √,
Bacterial Vaginosis ,Hepatitis C, Molluscum In Ireland
contagiosum √, NSU √
Suggested Reading

Sexually Transmitted Diseases Treatment
Guidelines 2002, MMWR, May 10,
2002/Vol.51/ No. RR-6, Available at
http:/www.cdc
 National Disease Surveillance Centre,
Annual Report 2001
Introduction STD`s in
Ireland

Overall rise in 2001 by 9.4%
 Most common 2001 Anogenital warts
 Syphilis Rose by 506.5%
 Hepatitis B by 160%
 Gonorrhoea, Genital Herpes and
Chlamydia trachomatis by over 20%
each
Chlamydia species

Order: Chlamydiales
 Family: Chlamydiaceae
 Genus: Chlamydia
 Four species: Chlamydia trachomatis, C.
psittaci, C.pneumoniae and C.pecorum
 Biovars: Trachoma and LGV
 Serovars: Trachoma 14(A-K), LGV
(L1.L2,L3)
Pathogenesis of Chlamydia
species

Obligate Intracellular organism, small nonmotile
 Consists of both RNA and DNA ,
ribosomes, cell wall and divide by binary
fission
 But lack peptidoglycan, lack ability to
produce own ATP, so energy parasites
 Implications for therapy, diagnosis
Pathogenesis of Chlamydia
species

Exists in 2 forms
 Elementary Body: extracellular, infectious,
metabolically inert, 300-350 nm
 Reticulate Body : non-infectious,
metabolically active, 800-1000nm
 Chlamydiae have a heat shock protein-?
Significance in serological tests
 LPS-2-keto-3-deoxyoctonic acid-genus
specific previously used in CFT and ELISA
tests
Genital Chlamydia Infection





Currently the most common bacterial sexually
transmitted infection (STI) in the UK and one of
the most common in Ireland, prevalence between
2 and 12%, in women attending GP`s
Genital chlamydial infection 1991-2001, increased
by 122%
Highest rates among 16-19 year old females
(791/100000) and 20-24 year old males
Although 34,000 in 16-19 yr 1999, estimated extra
100000 cases in that age group alone
Why?
Genital Chlamydia Infection

Caused by Chlamydia trachomatis
 If untreated can cause serious complications
 Those at risk , unprotected sexual
intercourse, esp. more than one partner and
those who change sexual partner
 Eye Infection: Inclusion conjunctivitis
CHLAMYDIA
Between 1991-2001 new episodes seen at GUM clinics in England
Rose 669,291 to 1,332,910 and increase 2000-2001 19% Chlamydial
Uncomplicated genital infection
CHLAMYDIA
Courtesy PHLS
Genital Chylamydial
Infection-IRL
Year 2001: 1649 confirmed cases vs 869 in 1999
Genital Chlamydia Infection

Transmission by unprotected sex or genital contact
( not casual contact)
 Pregnant women can pass it on to infants during
birth
 An infected person frequently has no symptoms
and may pass on infection to another
 Up to 50% of men and 70% of women are
asymptomatic initially
Genital Chlamydia Infection

Symptoms in women : unusual vaginal
discharge, bleeding between periods, pain
passing urine and lower abdominal pain
 Symptoms in men: discharge from penis,
burning and itching in the genital area, pain
passing urine
 Acute infection usually last a few days and
occur 1-3 weeks after becoming infected
Genital Chlamydia Infection





Serious effects on women if left untreated
One third of women with untreated chlamydia
go on to develop pelvic inflammatory disease
PID: Chlamydia can travel to salpinges and
ovaries and result in inflammation, 1/5 women
with an episode of PID will become infertile
It is the dominant infectious cause of chronic
pelvic pain, infertility and ectopic pregnancy
Incidence of EP in England 1/100000, accounts
for 21% of deaths resulting from complications
of pregnancy and childbirth
Genital Chlamydia Infection




Consequences of PID not
easily treated and life-long
consequences
An infected mother can
pass infection onto baby
resulting in eye
infection(4-10 days) and
pneumonia(4-12 weeks)
(treated with erythromycin
syrup and eye ointment)
Complications rarer in
men
Both may develop painful
arthritis
Genital Chlamydia Infection

Protection: reduce
number of partners
and use condoms
correctly and
consistently
 Lymphogranuloma
venerum-
Genital Chlamydia Infection





Diagnosis by urethral swab in male, endocervical
swab female and urine test, first void
In States use combined DNA Amplification for
Neisseria gonorrhoea and Chlamydia trachomatis
Now use Ligase Chain Reaction Test (LCR) or
Polymerase Chain Reaction (PCR)
However in the past chlamydial culture using cell
lines used
Testing for other STI`s should be carried out ,
ideally in GUM clinics
Genital Chlamydia Infection

Ideally diagnose early , as uncomplicated
chlamydial infection is easy to treat and
cure
 Doxcycline I00 mg bd for seven days or
azithromycin 1g-single dose
 All current and recent sexual partners( 60
days) of an infected person need to be tested
whether or not they have symptoms
C.trachomatis causing blindness
Gram Stain of Neisseria gonorrhoea
Neisseria gonorrhoeae
Year 2001: 349 confirmed cases
Neisseria gonorrhoeae

Limited to the columnar and transitional
epithelium
 In males: presents as acute purulent
discharge fron the urethra with dysuria 2-7
days after exposure
 Highly sensitive gram stain
 Very few are asymptomatic
Neisseria gonorrhoeae

In female: infection followed by mucopurluent
cervicitis which is often asymptomatic, some
vaginal bleeding post intercourse or d/c
 In 20% -endometritis,salpingitis with PID and
subsequent infertility and ectopic pregnancy
 Pharyngeal and anorectal lesions are usually
asympyomatic
 Conjunctivitis in newborn may cause blindness if
not rapidly and adequately treated
Neisseria gonorrhoeae

Septicaemia 0.5-1.0% -may develop
endocariditis, arthritis, skin
lesions,meningitis
 Arthritis usually polyarticular and may
cause permanent damage
 Strictly a human disease
Neisseria gonorrhoeae

Gram Stain
 Culture on selective
media e.g New York
City Media , plated as
soon as possible
 Confirm as
N.gonorrhoeae by two
different methods

Oxidase Positive
 Colistin Resistance
 Nitrate Reduction negative
 Acid only produced from
glucose
 Hydroxyprolylaminopepti
dase positive
 Antigen detection Test
 Sensitivity
Testing(Problem of
QRNG)
Neisseria gonorrhoeae

Period of communicability for months if
untreated
 Contact Tracing, Treatment
 Increased Risk of HIV infection
GC PHARYNITIS
GC OPHTHALMIA
NEONATURUM
Genital Herpes




Caused by Herpes simplex
virus(HSV)
HSV 1(30%) and 2
Primary or first episode is
often severe (2 weeks after
exposure), patient feels
unwell generally and often
gross inflammination with
vesciles around genitals or
anus, 2-4 weeks to resolve
Dormant phase , reside in
nerve supplying area- to
Reactivation with or
without symptoms
Genital Herpes

In 1999 17500 attending
with first attacks in UK
 Ireland 331 cases 2001
 20-24 age group, more
common in women
 Risk behavior
 Very infectious if
sores/vesciles present
 Infected women may pass
to virus onto their baby
during birth, neonatal
herpes potentially life
threatening, if present at
delivery requires
Genital Herpes





Diagnosis: viral culture of vesicle or HSV type
specific glycoprotein assays, must test for other
sexually td
Treatment : antiviral therapy(e.g acyclovir 400mg
tds for 7 days) , this reduces the length of severity
of infection
If frequent or severe recurrences , continuous
therapy may be required
More common now than 20yrs ago
Persons more susceptible to HIV infection
GENITAL WARTS

Veneral
Warts/Condylomata
acuminata
 Cause: Human
papillomaviruses(HPV)
 Site: Penis, anus, vagina
 Over 100 types identified,
1/3 genitally acquired
 2 nd Most Common STI
diagnosised in STD clinics
in UK and most common
Ireland (2001-3993)
HPV type 6,11
GENITAL WARTS

Same risk factors: unprotected sex, more
than one partner , frequently change
partners
 In 1999 70000 men attended STD clinics in
UK with first attack
 Age highest rates: women 16-24 and men
20-24
GENITAL WARTS





Infectious and 2/3 exposed will develop warts
within 3 months
An infected person may have no symptoms but
transmit the virus
In women they may occur inside vagina and on
cervix, around anus
Risk to Newborn rare
If untreated may take months or years to disappear
GENITAL WARTS

Serious health concern as some types particularly
HPV 16 and 18 associated with MALIGNANT
and PREMALIGNANT lesions of CERVIX( I.e.
Cervical Cancer)
– PREVENTION, ABSTINENCE, USING CONDOMS
AND REDUCTION OF PARTNERS
– TREATMENT: caustic solutions(Podofilox , TCAetc),
Freezing with liquid nitrogen , Surgery.
– May Recur even if treated
TREPONEMA

Order: Spirochaetales
 Family: Spirochaetaceae
 Genus: Treponema
TREPONEMA

VENERAL: Treponema pallidum
 Non-veneral treponematoses : yaws, bejel,
pinta
 Yaws: tropical rainforest
T.pertenue
 Pinta: Central america, Peru, Columbia,
Equator
 Bejel/Endemic syphilis: T.pallidum Middle
East, Russia, Turkey
EPIDEMIOLOGY

1999 USA 35,600 CASES , 556 CASES OF
CONGENITAL SYPHILIS
 Age group: 20-39 years, M:F RATIO 3:2
 2-5 FOLD INCREASE IN
TRANSMISSION OF HIV IF EXPOSED
Treponema

The spirochaetes causing these different
infections are micro-aerobic,
morphologically identical –tightly coiled
helical rods, 5-15 um long and 0.1-0.5 um
diameter- show only subtle antigenic
differences
SYPHILIS




Treponema pallidum
I ST isolated from
syphilitic lesions in 1905
STI, although may be
congenital or acquired
from blood transfusion
Untreated syphilis is a
progressive disease
SYPHILIS
Pathogenesis
T.pallidum enters tissues by penetration of
intact mucosae or through abraided skin
It rapidly enters the lymphatics
Widely disseminated through the bloodstream
and may lodge in any organ
Exact infecting dose not known but in animals
less than 10 organisms sufficient
SYPHILIS

The bacteria multiply at the initial entry site
and a chancre, a lesion characteristic of
primary syphilis forms after an average of 3
weeks
 Painless and usually on the external genitalia,
or cervix, anus, perianal, mouth
 Usually occur singly except in
immunocompromised
 Heals spontaneously 3-6 weeks and 1-12 weeks
later lesions of secondary syphilis occur
Primary chancre on the prepuce
Chancre of the retracted prepuce
Primary chancre of the vulva
Chancre of the glans
Chancre eroded, leaving an ulcer
Primary chancre of the lip
SYPHILIS

Time post exposure
 9-90 days
 6 weeks-6 months
(4-8 weeks after 1 lesion)
 2 years


4 years
3-20 years


Early( Infectious)
Primary
Secondary

Early(Latent)

Late( non-infectious)
Late(Latent)
Tertiary-Gummatous
-Cardiovascular
-Neurosyphilis



Secondary Syphilis




Variable- Malaise , fever,
sore throat
Skin with Macular or
pustular lesions,
particularly on trunk and
extremities
Lesions highly infectious
Gradually resolve and
period of latent infection
occurs I.e no clinical
manifestations but
serological evidence of
disease persists
Secondary Syphilis

Relapse of lesions
common so classifical
as early(likely) or late(
recurrence unlikely)
 Those with late latent
syphilis are generally
not infectious but may
transmit to fetus or
blood remains
infectious
Papulosquamous
syphilitic rash
Multiple condylomata lata lesions
Condylomata lata
Late or Tertiary

Decades after 1 syphilis is a slowly progressive
destructive inflammmatory disease that may
affect any organ
 3 most common forms are neurosyphilis,
cardiovascular syphilis and gummatous
syphilis- a rare granulomatous lesion of
skeleton , skin or mucocutaneous tissues
 Auto-immune pathology, isolation of organism
almost impossible
The lesion of
tertiary
syphilis – the
gumma
Late Syphilis

Not being able to coordinate muscle
movements
 Paralysis
 Numbness
 Gradual blindness
 Dementia
 Death
Gummatous lesion causing a
perforated palate
Charcot’s
arthropathy
Aneurysm
of the
ascending
aorta
Syphilitic alopecia of the eyebrow
Degeneration
of the
parenchyma
of the brain in
general
paralysis of
the insane
Congenital Syphilis

Depending on how long a pregnant women has
been infected , a good chance of stillbirth or a
baby who dies shortly after birth
 If not treated immediately a baby born without
symptoms can develop them within weeks
 Developmental delay or even seizures and
death
Hutchinson’s teeth
Syphilitic
snuffles
DIAGNOSIS

CLINICAL OBSERVATIONS
 CONFIRMED BY 2 METHODS
 SEROLOGY
 MICROSCOPY- DARK FIELD
-PHASE CONTRAST
DIRECT MICROSCOPY

Treponems visualised
directly in freshly
collected exudate from
Primarily or secondary
lesions
Rapid diagnosis but
insensitive(commensal
treponems) may use
immunofluorescence
SEROLOGICAL TESTS

After 3 weeks post infection antibodies
appear
 Non-treponemal Tests( non-specific)
antibody ,tests that react with antigen
cardiolipin
 Treponemal Tests(specific) antibody ,tests
that react with polypeptide antigen of the
treponem itself
SEROLOGICAL TESTS

Non-specific tests are easy to perform and
have low coat hence their use as a screening
method, however if positive must use a
specific anti-T.pallidum test( WHO criteria)
Non-Specific serological Tests

VDRL: mixture of cardiolipin, cholestrol
and lecithin, Ig M and IgG if present get
flocculation
 Positive in 70% primary and 99 % of
secondary syphilis
 Can quantitative
 Active infection
Non-Specific Tests

RPR: Rapid Plasma Reagin
 Quantitative
 May monitor therapy
 Over 50% -ve after 1 year if treated
Treponemal Specific Tests

T.pallidum particle agglutination test (TPPA):
Sera are pre-absorbed with non-pathogenic
treponeme to remove antibody against
commensalspirochaetes.Then if there is specific
antibody in the test sera it will bind to the
T.pallidum antigen coated onto the particles
resulting in agglutination-Quantitative
 Less sensitive 65% primary than FTA but same in
secondary and late syphilis
 Remains positive for Life
Treponemal Specific Tests





Fluorescent treponemal antibody absorbed –FTAabs:
Indirect immunofluorescence assay in which
T.pallidum is used as the antigen
Actone fixed treponemes are incubated with preabsored sera and bound antibody is detected with a
fluorescein-labelled conjugate and UV
microscopy.
Positive 80,100,95% of 1,2,late syphilitic
May remain positive after successful therapy
Treponemal Specific Tests
Enzyme –linked immunoabsorbent assay
(ELISA): Production of monoclonal antiT.pallidum antibodies has permitted their
development
 Can detect Ig M or IgG or both
 More efficient for large numbers being
screened
 Screening Method in SJH

LUMBAR PUNCTURE

Neurologic symptoms
 Treatment failure
 HIV +
 Other evidence of tertriary syphilis
 Very high titers
 Congenital Syphilis
Categories of Patients to be
Screened







Maternity/Obstetrics
HIV
GUM
Immigrants
Blood and organ
/tissue donors
Referred sera
Symtomatic patients





Combination of tests
used to make a
diagnosis
Dark Field
Microscopy
RPR
TPPA or ELISA
FTA ( Ig M and Ig G)
PROBLEMS





Both specific and non-specific can give falsepositive
VDRL may give a transient positive result
following strong immunological stimulus-e.g.
acute bacterial infection
Biological False positive in pregnancy
Autoimmune or connective tissue disease, in
drug users and hypergammaglobinaemia may
result in persistent false positive
Need to do additional tests
PROBLEMS

Yaws, leptospirosis pinta and relapsing
fever may give false positive
 Lyme`s disease produces antibodies that
react in the FTA and not VDRL
TREATMENT





If untreated 40% will eventually have
symptoms
Penicillin G, parenteral
No resistance seen
Late syphilis aqueous benzylpenicillin used as
better penetration into Central Nervous System
Jarisch-Herxheimer reaction
Syphilis Outbreaks








Reported in US, Antwerp and Manchester
In IRELAND 2001, 279 cases of primary and
secondary cases notified (year 2000 46)
97.2% 106 cases, associated with an outbreak
in Dublin
Majority cases male, 25 female
95% in 20-44 age group
80.8% early MSM, 47 bisexual, 59 heterosexual
~20% co-infected with HIV
Highest number diagnosised in JAN 2001
onwards
Syphilis Cases Graph
Syphilis Numbers
Courtesy NDSC
Outbreak Strategies

Outbreak Control Team
 Enhance Surveillance
 Case-Control Study
 Awareness promotion about PREVENTIVE
Measures esp. MSM
 Known contacts have serology repeated at 3
months to outrule false negatives
 Out Reach Clinics
TRICHOMONIASIS

Cause: Trichomonas
vaginalis
 Site of Infection:
Vagina, Urethra
 Men can acquired
from infected women
only usually
 Women can acquire it
from women or men
TRICHOMONIASIS



Most common curable
STD in young women in
USA
Most men no symptoms ,
irritation inside penis ,
slight discharge or burning
Women many have a
frothy , yellow green
vaginal discharge with a
strong odour, discomfort
during intercourse
TRICHOMONIASIS





Symptoms 5-28 days post exposure
Complications: In pregnant women may cause
premature rupture of membranes and preterm
delivery
Increases risk of acquiring HIV if exposed
Treatment: one dose metronidazole, symptoms
disappear in a few weeks, treat both partners
Prevention
HIV INFECTION

UN report 43 million wordwide-Nov 2002
 Epidemiology in Ireland
 Culmulative Dec 2002 3009 cases
 In 2001, 299, in 2002 364 cases
Heterosexual
63.5%
Age F 20-29 mostly
M 30-39
MSM
13%
Children 8 cases.
119 born to HIV
Mothers
IDU-14%
Year 2002: 364
Link STD`S AND HIV
THOSE INFECTED
STD`S ARE AT
LEAST 2-5 TIMES
MORE LIKELY THAN
UNINFECTED PERSONS
TO ACQUIRE HIV
IF THEY ARE
EXPOSED TO THE VIRUS
BY SEXUAL CONTACT
WHY?
HOW TO PREVENT
Samples to be sent for STI`s
CONTROL OF STD`S

PREVENTION
 SCREENING
 CONTACT TRACING
 ? ROLE FOR GENERAL SCREENING