Sexually Transmitted
Diseases
Dr Syed Suhail Ahmed
Incidence and spread of STD are greatly influenced by
numerous factorsMultiple sexual partners
 Increasing density and frequent movement of
people within population
 Absence of vaccines for most STD s.
 Asymptomatic infection – a pt with an STD may be
free of symptoms especially females. They may
serve as reservoir of infection and unknowingly
spread the pathogen.
Bacterial agents 1.Chlamydia tracomatis (D - K serotypes & L1 L2 L3
Serotypes)
2. Neisseria gonorrhoeae
3. Treponema pallidium
4. Haemophilus ducreyi
5. Gardnerella vaginalis
6. Calymmatobacterium granulomatis
7. Mycoplasma, Ureaplasma( t strains).
Viral agents 1.Human papilloma virus
2. Herpes simplex virus types 1 &2.
3. HIV
4. Hepatitis B virus
5. Molluscum Contagiosum
Protozal agents- Trichomonas vaginalis, Giardia
lamblia
Fungal agents – Candida albicans
Ectoparasites- Phthirus pubis, Sarcoptes scabiei
Neisseria gonorrhoeae :
Gonococcus was first described in gonorrheal pus by
Neisser.
MorphologySize - 0.6- 0.8 Microns
Shape - adjacent sides concave, kidney shape
Arrangement - pairs(diplococci)
Nonmotile ,Nonsporing
Staining reaction –
Gram staining : Gram negative oval or spherical cocci.
Gram stained smear of urethral discharge showing;
Gm-ve diplococci intra- & extra-cellularly
in pus cells (diagnostic)
Gram stained film of Neisseria gonorrhoeae culture
on Chocolate agar showing;
Gram-ve diplococci (kidney shaped)
Cultural characteristic :
Facultative intracellular parasite.
Aerobes but may grow anaerobically
Temperature- 35-37 c
Grows best in 5-10% CO2
Growth - 24- 48 Hrs
MediaEnriched media – Chocolate Agar(sterile site)
Selective media- Thayer Martin medium, New york
city media.
colonies (T1-T5) are small round, transparent or
opaque and easily emulsifiable.
Transport media- Stuarts or Amies Transport media
Biochemical Reaction : Several biochemical test like
N.gonorrhoeae ferment only glucose with
production of acid.
Catalase - Positive
Neisseria are oxidase positive key test for identifying
them.
Antigenic structure : (VIRULENCE FACTOR)
Neisseria gonorrhoeae is antigenically
heterogenous and capable of changing its surface
structure to avoid host defenses. Surface structures
include the following
A. Pili – Hair like appendages that enhance
attachment to host cells and resistance to
phagocytosis.
B. OPA- this protein function's in adhesion of
gonococci within colonies and in attachment of
gonococci to host cells.
C. lipooligosaccharides(LOS) – In contrast to GNR
gonococci have LOS. Toxicity in gonococal infection
is largely due to endotoxin effect. The LOS
structurally resemble Human cell membrane
glycospingolipids ( molecular mimicry),this helps
gonococci evade immune regulation.
D.IgA1 protease- splits and inactivate IgA1.
Pathogenesis –
Mode of infection : The disease is acquired by sexual
contact with an infected partner.
Incubation period - 2-8 days
Mechanism :
1.Extracellular multiplication : Upon gaining access to
the cervix or urethra by sexual contact, these
organism subvert the humoral immune response by
antigenic variation of surface molecules or by
production of IgA1 protease.
2. Attachment – Attach to nonciliated ,low coloumnar
epithelial cell that is mediated by Pili or OPA.
3. Endocytosis – Followed by penetration of the
organism between and through epithelium of the
submucosal tissue, membrane bound endocytic
vesicle is formed and host killing is inhibited by the
Outer membrane protein.
4.Transport - Next the membrane bound vesicle
containing multiple organism, migrate close to the
basal surface of epithelial cell.
5.Exocytosis - Fusion of the basal membrane and
vesicular membrane ensues, followed by exocytosis
of gonococci.
Host inflammatory response is mostly seen.
Clinical significance Genital infection in menAcute Uretheritis – Mucopurulent discharge
containing gonococci in large nos. the infection
extends along the urethra to the prostrate, seminal
vesicles and epididymis. Fibrosis occur leading to
urethral stricture. The infection may spread to
periurethral tissues, causing abscess and multiple
discharging sinus.
Genital infection in women : Primary infection is in
endocervix and extends to urethra and vagina
giving rise to mucopurulent discharge .It may then
progress to uterine tubes, causing salpingitis ,
Fibrosis & obliteration of the tubes.
Infertility occurs in 20 % of women with gonococcal
salpingitis.
Men & Women
Rectal Gonococcal infection – Proctitis occurs in both
sex. It may directly spread in women but in men is
the result of anal sex.
Pharyngeal infection - Oral Sexual exposure.
Disseminated Gonococcal infection - Gonococcal
bacteremia leads to skin lesions ,arthritis and very
rarely meningitis.
Nonveneral infection – Gonococcal Ophthalmia in
the newborn which result from direct infection
through birth canal(Conjuntivitis).
• Lab diagnosis 1. Microscopy – Examine Gram Stain smears of
urethral discharge from men and urethral and
cervical secretion from women .The observation of
characteristic kidney shaped, gram negative
diplococci lying within polymorphnuclearleukocytes
with few extracellular organism is typical of
gonococcal infection.
2. Culture – Plate out the specimen on Enriched
media like chocolate agar and on selective culture
media like Thayer martin media ,MTM, New York
City media. Incubate at 35- 37 c in Co2 enriched
atmosphere.
• Presumptive colonies of nesisseria can be identified
by G.S and oxidase test.
• RCUT OTHER biochemical test.
3. Antigen detection – ELISA,DNA Probe assay
Fluorescent antibody test.
CHLAMYDIA TRACOMATIS
 Small Obligate intracellular parasite.
 lack mechanism for production of metabolic
energy and cannot synthesize ATP.
 They have the typical LPS of GNB.They lack
pepitodoglycan layer.
 Dimorphic growth cycle.
 The genus Chlamydia comprise 4 sp
C. tracomatis
C. pneumonia
C. psittaci
C. pecorum
• Structure –
•
C.tracomatis are small , nonmotile bacteria.They
have the typical LPS of GNB . They exhibit dimorphic
growth cycle • Elementary bodies- EB are small electron dense
structure about 300- 350 nm in diameter. They are
extracellular, environmentally resistant,
metabolically inert, infectious structure.
• Reticulate bodies- RB are 0.5- 1 micron, is devoid of
any electron dense nucleoid. They are large
pleomorphic structure ,metabolically active and
divide by binary fission, they are non infectious.
• Staining –
Gram Staining : Gram reaction of Chlamydia is
negative and variable and is not useful in
identification of these agents.
Giemsa stain – ED – purple RB – blue.
• Antigens1.LPS–common to all Chlamydia(group sp antig)
2.Outer membrane protein( sp or serovar sp) Based
on OMP antigenic differences Serovars of
C.tracomatis are grouped by letter.
A - C tracoma
D - K nongonoccal urethritis, epididymitis cervicities,
C. Trachomatis culture on McCoy cells
Giemsa stained showing large chlamydial inclusions
partially obscuring the nuclei
• PathogenesisSource of infection - Humans ,this organism is
maintained within population largely as a
consequence of asymptomatic infection of men and
women.
Mode of infection – Sexual contact.
Mechanism – The mechanism by which C.tracomatis
induces inflammation and tissue destruction are
poorly understood.
1. On sexual exposure E.B pass from one infected
individual to uninfected individual.
2. They quickly adsorb to the microvilli of coloumnar
epithelial cells.
• They are endocytosed within membrane bound
vesicles(inhibits fusion of infected endosome with
lysosomal granules.
• Within the endosome, EB converts to metabolically
active RB and multiply.
• this intraendosomal inclusion are referred to as
inclusion bodies.
• When the cellular nutrients have been depleted the
RB convert to EB and are either exocytosed into the
extracellular space or are liberated by cell lysis
infecting adjacent cell (72 -96hrs).
• Damage from chlamydial infection is largely due to
acute inflammatory response in the area of
infection and scarring of the host tissue after
infection. The acute inflammatory response may be
consequence of the LPS produced by C.tracomatis.
• Clinical signifance-
Site of infection Disease
Eye
Trachoma
Inclusion
conjunctivitis
ophthalmia
neonatorum
Male Genital
tract
Female Genital
Tract
Male & female
Organism(serovars)
C.Trachomatis(A,B,C)
C.Trachomatis(D-K)
C.Trachomatis(D-K)
Non specific urethritis C.Trachomatis(D-K)
proctitis&epididymitis
Cervicitis,urethritis,en
dometritis,salpingitis, C.Trachomatis(D-K)
PID,perihepatitis,abor
tion,infertility
C.Trachomatis(L1–
LGV
L3)
• Lab diagnosis of C.tracomatis 1. Cell culture - Mccoy cells are commonly used. After
48 -72 hrs of incubation monolayers are stained
with iodine or an immunofluorescent stain and
examined microscopically for inclusions.
2. Direct antigen detection –
 Immunofluorescence DFA – FITC monoclonal
antibody to either outer membrane protein or
lipopolysaccharide of C.tracomatis in smears of
samples.
 ELISA.
C. trachomatis immunofluorescence
IF of cervical smear showing apple-green fluorescent
C. trachomatis elementary bodies
3. Serologic Diagnosis - Microimmunofluorensence
assay, CFT.
4. Molecular techniques- PCR, Ligase Chain reaction
and Transciption mediated amplification
Treponema Pallidium
• Members of the genera treponema borrelia are
spirochaetes belonging to the family
spirochaetaceae. Treponema cause the following
diseases1. Veneral syphilis- T. pallidium
2. Endemic syhilis - T. pallidium endemicum
3. Yaws
-T.pertune
4. Pinta
- T.carateum
• StructureThis organism are slender, tightly coiled spiral shape
5-15 nm long and 0.1-0.2 micron width. Actively
motile .Non cultivable.
Staining reaction - they do not stain by gram method
modified staining procedure are used like silver
impregnation methods or Fontana s method. They
can be seen in dark field illumination.
Ultrastructurally ,the cytoplasm of T.pallidium is
surrounded by trilaminar cytoplasmic membrane
enclosed by a cellwall containing pepitodoglycan
which gives cell rigidity and shape.
• Several flagella are attached at each pole of the cell
and wraps around bacterial cell body.
• The outer membrane is usually lipid rich.
•
•
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PathogenesisSource of infection- Natural infection with T.
pallidium occurs only in human beings.
Mode of infectionSexual contact.
Congenital syphilis occurs following vertical
transmission and also during passage through
infected birth canal.
Transfusion of blood.
• Virulence factor Molecular mimicry outer sheath contain
glycosylaminoglycans which resemble molecules
found on the surface of human cell
 Hyaluronidase – breakdown of hyaluronic acid in
host tissue
• Mechanism1 . T. pallidium following deposition onto the genital
mucosa, gain access to subepithelial tissue through
tiny cracks in the epithelial cell space.
2. From this site T. pallidium spreads to local
lymphnodes eventually to the blood over a period
of 10 wks.
3. After an incubation period of 2-10 wks, a painless
syphilitic chancre characteristic of primary syphilis
develops at the site of infection due to
inflammation and necrosis resulting from response
by neutrophils, T-cells and macrophages.
4. The microorganism then disseminates in the the
blood ,localized to bood vessel and spreading to
skin, liver ,joints ,lymphnodes ,muscles and brain.(
Secondary syphilis).
5.Following secondary syphilis ,the disease progress
into a state of latency, microorganism resides
within local lymphnodes and the spleen.
6.In 30-40% of latent pts,the pathogen reactivates &
begins to replicate actively,spread & penetrate
various tissues of the body.
7.Tertiary syphilis,gumma formation appears to be the
result of Cell mediated hypersensitivity reaction to
treponemal antigen.
• Clinical manifestation • Primary syphilis - chancre at the site of inoculation
external genitila mostly in males.
• Cervix ,mouth ,perinal area and anal canal in
females.
• Chancer or ulcer – no exudates, painless indurated
hard chancre .the chancre heals on its own within 36 wks leaving either no trace or a thin atrophic scar.
• Secondary syphilis - disseminated syphilis
It is the most florid stage of infection. It results from
multiplication and dissemination of the spirochaete
and last until a sufficient host response to exert
some immune control over the spirochaete .it
usually begins 2-8 wks after the appearance of a
chancre.
Latent syphilis - After the secondary lesion disappear
there is a period of quiescence known as latent
syphilis. diagnosis during this period is possible only
by serological test. In many cases, this is followed by
natural cure but in some leads to manifestation of
tertiary syphilis appears
• Manifestation of Secondary Syphilis
• Manifestation of Skin
Rash,Macular,Maculopapular,,papular,Pustular
Pruritus
Mouth and throat
Mucous patches ,Erosions ,Ulcer (aphthous)
Genital lesions
• Chancre
• Chondyloma latum
Generalized lymphadenopathy
• Tertiary syphilis (late syphilis) these consist of
cardiovascular lesions including aneurysm ,chronic
granulomata and meningovascular manifestation. In
few cases ,neurological manifestation such as tabes
dorsalis or general paralysis of insane develops
several decades.
• Congenital syphilis - Transplacental transmission
can take place at any stage of pregnancy .a woman
with early syphilis can infect her fetus much more
commonly .
• Lab diagnosis of T. pallidium
• 1.Microscopy
• A. Dark field examination- A drop of exudate is
placed on a slide and preparation is examined
under dark field illumination for typical motile
spirochaetes.
• B.DFA-TP - A drop of exudate is placed on a slide
with flourescent labelled anti treponemal serum
and examining by means of flourescent microscope.
• Serological test - This test forms the main stay of
laboratory diagnosis. Various methods use to
measure anti body response in treponemal
infection can be divided into two types:
• A: Test to measure antibodies against non specific
treponemal antigen.
• B:Test to measure antibody against antigens specific
for pathogenic treponemes.
• A- Non treponemal antigen test• Non specific test: this test use the lipoidal or
cardiolipin antigen. they are commonly used test.
• VDRL or RPR
• Primary syphilis - 70%
• Secondary syphilis - 100%
• Positive VDRL revert to negative after treatment
• B.Specific treponemal test
• 1.FTAbS(flourescent treponemal antibody
absorbtion test)the serum is first absorb in the
suspension of non pathogenic treponemes which
removes non specific cross reactive anti bodies that
may be directed against commensal spirochaetes.
• Primary syphilis 80%
• Secondary syphilis 100%
• Late syphilis 95%
• TPHA (MHATP)- Antigen is coated on the surface of
red cells and specific antibody in test sera causes
heamagglutination.
• ELISA ,Blotting etc.
• 3. PCR