STD ways of transmission Prognosis Diagnosis Type's of disease Treatment Vaccine

1. SEXUALLY TRANSMITTED
DISEASES

2. CLINICAL CASE
 A 50-year-old man visits a clinic because he has an
ulcerous lesion on the shaft of his penis. The lesion
is painless and hard to the touch (refer to figure
below). A dark-field microscope visualized the
etiologic agent in a sample taken from the lesion

3. TREPONEMA PALLIDUM: MORPHOLOGY
T. pallidum on election microscopy shows a trilaminar
cytoplasmic membrane surrounded by a cell wall. The
latter contains peptidoglycan that confers the cell its
shape and rigidity. The cell wall is surrounded by an
outer membrane layer.

4. TREPONEMA PALLIDUM: MORPHOLOGY
These endoflagella do not
extend beyond the cell wall
outside but remain always
confined within the outer
membrane layer
Three (four) flagella
known as endoflagella,
responsible for motility
of bacteria, originate
from each end of the cell
and extend toward the
opposite end of the cell
in the space between
cell wall and outer
membrane layer.

5. TREPONEMA PALLIDUM : ANTIGENIC
STRUCTURE
 Cardiolipin antigen
This hapten elicits the production of an antibody, known as
reagin antibody
 T. pallidum group-specific antigen
is protein in nature. It is found in T. pallidum as well as in
nonpathogenic cultivable treponemes, such as Reiter’s
treponeme. Reiter’s protein complex complement
fixation test
 T. pallidum species-specific antigen
is probably polysaccharide in nature. The specific
treponemal test, such as T. pallidum hemagglutination
(TPHA) test, detects antibodies by using these antigens.

6. TREPONEMA PALLIDUM : VIRULENCE
FACTORS
Virulence factors Biological functions
Outer membrane proteins Promote adherence of T.
pallidum to the surface of
host cells
Enzyme hyaluronidase Facilitates perivascular
infiltration
Fibronectin Prevents phagocytosis of
T. pallidum by
macrophages

7. TREPONEMA PALLIDUM : PATHOGENESIS

8. PRIMARY SYPHILIS
 The hard chancre
develops after an
incubation period of
approximately 3 weeks
and will usually heal
within 3–6 weeks.
Regional
lymphadenopathy may
persist for months,
despite healing of the
chancre.
8

9. SECONDARY SYPHILIS
 The manifestations of secondary
syphilis usually begin 6–8 weeks
after the appearance of the initial
chancre and may overlap the time
when the primary chancre is
present. The principal
manifestations of secondary syphilis
are skin and mucous membrane
lesions as well as manifestations of
systemic disease.
9

10. SECONDARY SYPHILIS
 Systemic manifestations include
malaise, anorexia, headache,sore
throat, arthralgia, low-grade fever,
and generalized lymphadenopathy.
The skin and mucous membrane
lesions occur over the entire body
and are usually macular, but can be
papular or nodular. These lesions
are also found on the palms and
soles.
 The first stage of secondary syphilis
lasts 2–6 weeks, and the patient
then enters the latent phase.
10

11. TERTIARY, OR LATE, SYPHILIS
 Tertiary, or late, syphilis is a noncontagious but
highly destructive phase of syphilis that
develops over many years.
 The manifestations may appear as early as 5
years after infection but characteristically
occur after 15 to 20 years. The manifestations
depend on the body sites involved
 Tertiary syphilis presents in three basic forms:
 gummatous syphilis (granulomatous lesions
may be found in the skin, bones, and mucous
membranes with other mass-producing
lesions, such as tumors.),
 cardiovascular syphilis, and
 neurosyphilis.
11

12. NEUROSYPHILIS
The most common entity is a chronic meningitis with fever,
headache, focal neurologic findings, and increased cells
and protein in the cerebrospinal fluid (CSF).
Cortical degeneration of the brain causes mental changes
ranging from decreased memory to hallucinations or frank
psychosis. In the spinal cord, demyelination of the posterior
columns, dorsal roots, and dorsal root ganglia produces a
syndrome called tabes dorsalis, which includes ataxia,
wide-based gait, foot slap, and loss of the sensation. The
most advanced central nervous system (CNS) findings
include a combination of neurologic deficits and behavioral
disturbances called paresis, which is also a mnemonic
(personality, affect, reflexes, eyes, sensorium, intellect,
speech)
12

13. CARDIOVASCULAR SYPHILIS
 is due to arteritis involving the vasa vasorum of the
aorta and causing a medial necrosis and loss of
elastic fibers. The usual result is dilatation of the
aorta and aortic valve ring. This in turn leads to
aneurysms of the ascending and transverse
segments of the aorta and/or aortic valve
incompetence. The expanding aneurysm can
produce pressure necrosis of adjacent structures or
even rupture
13

14. TREPONEMA PALLIDUM : CLINICAL
SYNDROMES
1. Venereal syphilis (transmitted by sexual contact)
2. Nonvenereal syphilis (congenital syphilis and
occupational syphilis)

15. CONGENITAL SYPHILIS
 Congenital syphilis results when
maternal syphilis is transmitted in
utero to the fetus after 16 weeks’
gestation. If the mother is highly
infective, the infant will be stillborn or
present with early congenital syphilis
manifested during the first 2 years of
life by rhinitis (snuffles). Rhinitis is
followed by skin and mucocutaneous
lesions similar to those of an adult
with secondary syphilis and by
osteochondritis, hepatosplenomegaly
and lymphadenopathy, immune
complex-induced glomerulonephritis,
or death.
15

16. CONGENITAL SYPHILIS
 Late congenital syphilis occurs in
children after age 2. Manifestations
include Clutton joints (painless
symmetrical hydrarthrosis of the knee
joint), deafness, Hutchinson teeth
(notched and narrow edged
permanent incisors) and
mulberryshaped molars, and bone
abnormalities that include saddle
nose, saber shins, and rhagades
(fissures, cracks, or fine linear scars
in the skin especially around the
mouth)
16

17. TREPONEMA PALLIDUM : EPIDEMIOLOGY

18. TREPONEMA PALLIDUM :
LABORATORY DIAGNOSIS
 Microscopy
 Direct antigen detection
 Serodiagnosis:
 Nontreponemal tests (measure antibody directed against
cardiolipin, a lipid complex so called because one
component was originally extracted from beef heart.
Anticardiolipin antibody is called reagin, and the tests that
detect it depend on immune flocculation of cardiolipin in the
presence of other lipids. Standard tests of syphilis: STS):
 Wasserman complement fixation test
 VDRL test
 Rapid plasma reagin (RPR) test
 Treponemal tests - detect antibody specific to T pallidum :
 T. pallidum immobilization test
 T. pallidum agglutination test
 T. pallidum immune adherence test
 Fluorescent treponemal antibody test
 Enzyme immunoassay

19. SYPHILIS SEROLOGY
The time course of treponemal and nontreponemal tests in
treated and untreated syphilis is shown. The nontreponemal
test results (VDRL, RPR) rise during primary syphilis and reach
their peak in secondary syphilis. They slowly decline with
advancing age. With treatment, they revert to normal over a few
weeks. The treponemal tests (FTA-ABS, MHA-TP) follow the
same course but remain elevated even after successful
treatment
19

20. TREPONEMA PALLIDUM :
LABORATORY DIAGNOSIS

21.  Penicillin for primary and secondary syphilis;
 tertiary syphilis not treatable;
 Prevention of disease: Abstinence, mutual
monogamy, condom usage for syphilis; avoid contact
with patients with other diseases
21
TREATMENT AND PREVENTION

22.  A 22-year-old female complained of lower
abdominal pain on and off for the last 3 months.
She complained of a feeling of heaviness in the
pelvis and pain during sexual intercourse. On
examination, a tender mass was found to the right
side during examination. Gram staining of cervical
swab showed plenty of pus cells and a few Gram-
negative cocci. She gave a history of allergy to
penicillins.
CLINICAL CASE

23. NEISSERIA GONORRHOEAE:
MORPHOLOGY
N. gonorrhoeae is a small gram-
negative diplococcus that has
flattened surfaces between the
adjacent individual cocci
(shaped similar to a kidney bean
or a coffee bean).

24. NEISSERIA GONORRHOEAE: VIRULENCE FACTORS

25. NEISSERIA GONORRHOEAE: PATHOGENESIS
The pathogenesis of
gonorrhea is related to the
ability of gonococci to
attach to mucosal cells via
their pili and then
penetrate to submucosal
areas to induce a strong
influx of
polymorphonuclear
leukocytes

26. NEISSERIA GONORRHOEAE: CLINICAL SYNDROMES
a) gonorrhea,
b) disseminated gonococcal
infections (DGI),
c) ophthalmia neonatorum, and
d) other gonococcal diseases

27. CLINICAL MANIFESTATIONS
27
A patient with gonococcal urethritis.
The urethra was stripped with a thin
sterile urethral swab. The swab was
inserted into the urethra, rotated, and
pulled toward the orifice of the urethra
to express purulent material
A skin lesion on a patient with a
disseminated gonococcal
infection
A newborn with ophthalmia
neonatorum, an infection of the
eyes due to Neisseria
gonorrhoeae

28. NEISSERIA GONORRHOEAE: LABORATORY
DIAGNOSIS
Diagnosis of gonorrhea involves a threefold
approach.
1. Evaluation of the patient’s presenting
signs and symptoms and sexual history.
2. Gram stain of a smear of the patient’s
purulent exudate. The smear is positive
for gonorrhea if gram-negative diplococci
are seen within polymorphonuclear
leukocytes.
3. Culture exudates for N. gonorrhoeae
using Thayer-Martin medium (chocolate
agar containing vancomycin, colistin, and
nystatin)
or testing the exudates for N. gonorrhoeae
infection by nucleic acid amplification
techniques

29. TREATMENT AND PREVENTION
 cephalosporins
 quinolone
 The drugs of choice are ceftriaxone or ciprofloxacin
 Plus azithromycin or doxycycline
 Preventing transmittal requires improved education of
sexually active individuals, proper reporting, follow-up of
patients and their contacts, use of condoms, and
chemoprophylaxis to prevent ophthalmia neonatorum.
Culturing pregnant women for gonorrheal infection
before delivery and treating those who are infected can
prevent gonorrheal infections of the newborn.
29

30.  A 6-year-old boy attended the Ophthalmology OPD
with symptoms of conjunctivitis of the right eye.
Examination showed follicular hypertrophy with
diffuse inflammation that had affected the entire
conjunctiva along with pannus formation. Iodine
staining of conjunctival scrapings demonstrated
inclusion bodies of Chlamydia trachomatis. The
condition was diagnosed as trachoma.
CLINICAL CASE

31. CHLAMYDIA TRACHOMATIS:
MORPHOLOGY
 Chlamydiae are
obligate intracellular
parasites of humans
and animals with
marked affinity for the
squamous epithelial
cells of the
gastrointestinal and
respiratory tracts.

32. HUMAN INFECTIONS CAUSED BY CHLAMYDIA
SPECIES
32

33. LIFE CYCLE
33

34. Elementary body Reticulate body (initial body)
Size about 0.3 µm Size 0.5-1.0 µm
Rigid cell wall Fragile cell wall
Adapted for extracellular survival Adapted for intracellular growth
Isolated organisms infectious Isolated organisms not infectious
RNA:DNA content = 1:1 RNA:DNA content = 3:1
Toxic for mice Nontoxic for mice
Relatively resistant to sonication Sensitive to sonication 34

35. CHLAMYDIA TRACHOMATIS: ANTIGENIC
STRUCTURE
 Genus-specific antigen
heat-stable, complement-fixing. It is an LPS–protein complex
resembling the LPS of Gram-negative bacilli. It is present in EBs
and RBs.
 Species-specific antigen
is present at the envelope surface
 Serotype-specific antigen
is present only in a few species of chlamydiae. They are located in
the major outer membrane proteins (MOMPs) and are useful for
intraspecies typing of Chlamydia species
 Typing of species
 trachoma biovar causing trachoma and inclusion conjunctivitis
(TRIC) – 13 serotypes,
 lymphogranuloma venereum (LGV) biovar causing LGV – 5
serotypes, and
 serovars causing pneumonitis

36. CHLAMYDIA
TRACHOMATIS:
VIRULENCE FACTORS
 The ability to multiply intracellularly in the infected cell is
the key mechanism of virulence of C. trachomatis.
 The bacteria prevent fusion of phagolysosome with cellular
liposomes, thereby preventing intracellular killing of the
bacteria by the host cell.
 Repeated infections caused by C. trachomatis contribute to
pathology seen in the infected eye in trachoma.

37. C. trachomatis causes disease mainly by
(a) direct destruction of infected host cells during multiplication and
(b) inducing inflammatory responses in the host.
C. trachomatis enters the host through minute abrasions or injuries in the
skin.
The bacteria react specifically with the receptors that are found on the non-
ciliated epithelial cells (they are typically found on the mucous membranes
of the conjunctiva and genitourinary system, such as urethra, endocervix,
endometrium, fallopian tube, and respiratory tract).
The LGV biovar multiplies in mononuclear phagocytes found in the
lymphatic system. The pathological lesions are typically found in the lymph
nodes draining the site of primary infection. Granuloma is characteristic
pathological lesion. Subsequently inflammatory process spreads to other
surrounding tissues and finally rupture of the lymph nodes leads to the
formation of abscess or sinus tracts. Infections with trachoma serovars are
associated with severe inflammatory reaction consisting of neutrophils,
lymphocytes, and plasma cells
37
CHLAMYDIA TRACHOMATIS: PATHOGENESIS

38. CHLAMYDIA TRACHOMATIS: CLINICAL
SYNDROMES
 Lymphogranuloma venereum
 Ocular LGV
 Trachoma
 Adult inclusion conjunctivitis
 Neonatal conjunctivitis
 Infant pneumonia
 Urogenital infections

39. CHLAMYDIA TRACHOMATIS: CLINICAL
SYNDROMES

40. IMMUNITY
 To C.trachomatis infections seems to take a long time
to develop and even then is incomplete. Up to 50% of
women with genital infection may still be shedding the
organism a year later. The intracellular location and the
prospect that low levels of cytokines may induce the
persistent state are complicating features.
40

41.  Demonstration of C. trachomatis by smear or culture
requires the collection of epithelial (not inflammatory) cells
from the site of infection (conjunctiva, urethra, cervix).
 Culture is carried out in specially treated cells in which
chlamydial inclusions are detected by immunofluorescence.
Results require incubation for 3 to 7 day
 Direct fluorescent antibody (DFA) and immunoassay
methods have also been developed.
 All these methods have now been replaced by the newest
generation of nucleic acid amplification (NAA) tests. 41
CHLAMYDIA
TRACHOMATIS:
LABORATORY
DIAGNOSIS

42.  Culture or DFA are now reserved
for pharyngeal and rectal
specimens which for NAA tests
might generate false positives.
 Nucleic acid amplification
methods for genital Chlamydia
infection are now combined with
parallel tests for N. gonorrhoeae
42
CHLAMYDIA TRACHOMATIS: LABORATORY
DIAGNOSIS

43.  Serodiagnostic methods have
limited use in diagnosis because
of the difficulty of distinguishing
current from previous infection
although detection of IgM
antibodies against C. trachomatis
is helpful in cases of infant
pneumonitis. Chlamydial serology
is also useful in the diagnosis of
LGV, where a single high
complement fixation antibody titer
(higher than 1:32)
43
CHLAMYDIA TRACHOMATIS: LABORATORY
DIAGNOSIS
A direct fluorescent antibody
test for Chlamydia trachomatis.
The bright red color reveals the
presence of Chlamydia within
cells; this result is diagnostic for
a C. trachomatis infection.
Green indicates human cells

44. TREATMENT AND PREVENTION
 azithromycin or doxycycline
 infected women with azithromycin late in pregnancy
 Chlamydial genital infections are prevented by
using safe sexual practices and by prompt
treatment of symptomatic patients and their
partners
44