Microorganism that

cause Sexually
Transmitted Diseases

Efrida Warganegara
 SEXUALLY TRANSMITTED (VENEREAL)
DISEASES
 Sexually Transmitted Diseases (STD) / Venerial
Diseases (VD) : infections that are often, if not
always, passed from person to person contact.
 A wide variety of infectious microorganism can
be spread by sexual contact range from micros
viruses (HIV) to visible insect (pubic louse)
 STD usually result from having vagina, oral and
anal sex with an infected partner (occasionaly
transmitted by kissing or close body contact)
 Agents of some STD may be transmitted  food,
water, blood transfusion, contaminated medical
instruments, needles use by injecting drug users
 Bacterial Sexually Transmitted Infections
 Neisseria gonorrhoeae
 Yeasts and fungi
 Chlamydia trachomatis
 Treponema pallidum  Candida albicans
 Haemophilus ducryei (chancroid)  Candida glabrata
 Lymphogranuloma  Candida tropicalis
 Mycoplasma
 Ureaplasma  Parasites
 Calymmatobacterium granulomatis  Trichomonas
 Gardnerella vaginalis
vaginalis
 Viruses
 Entamoeba
 Herpes simplex II
histolytica
 Hepatitis B
 Hepatitis C
 Giardia lamblia
 HIV  Sarcoptes scabiei
 Papillomavirus  Phitirius pubis
 CLASSIFICATION OF STD
 Traditionally, five disease have been
clasification as STD (Earliest): Syphilis,
Gonorrhea, Chancroid,
Lymphogranuloma Venereum (LGV) and
Granuloma Inguinale.

 However, many others diseases are

sexual transmitted, including : Genital
Herpes, Hepatitis, Moluscum
Contagiosum, Scabies, and HIV
infection, which cause AIDS
 Bacterial Sexually Transmitted Diseases
Prominent Complications
Organism Complication
Clinical Feature in Pregnancy
Pelvic Newborn
Neisseria
Urethritis inflammatory conjunctivitis
gonorrhoeae
disease; arthritis (severe)
Chlamydia Pelvic Newborn
trachomatis Urethritis inflammatory pneumonia or
serotypes D-K disease conjunctivitis
Chlamydia
Genital fistulas,
trachomatis Regional
ulcers, and …
(lymphogranuloma adenopathy
elephantiasis
venereum)
Congenital
Nerve; aorta; brain
Treponema Hard chancre, infection causing
damage of tertiary
pallidum primary stage stillbirth or birth
stage
defects
Haemophilus Soft chancre with
… …
ducreyi multiple ulcers
Group B Mild genital tract Fulminant
…
streptococci infection meningitis in baby
 CLASSIFICATION OF STD
 STD are sometimes grouped by symptoms and
sign they cause.
 Syphilis, Genital Herpes and Chancroid -> all
cause Ulcers (sores) on the skin or membranes
lining the vagina or mouth.
 Both Gonorrhea & Chlamydial infections cause :
- In Men : Urethritis (inflamation & discharge of
the urethra)
- In Women : Cervicitis (inflamation & discharge
of the urethra), and Pelvic infections
- In Newborn : Eye infectons
Type of Infections Infectious Agents
Inflamatory (Exudative Infections)
Neisseria gonorrhoeae (Gonorrhoeae)
Urethritis, Cervicitis
Chlamydia trachomatis (NGU or
Cervicitis)
Mycoplasma hominis, Mycoplasma
genitalium
Vaginitis Trichomonas vaginalis (trichomoniasis)
Candida albicans (Candidiasis)
Gardnerella/ Mobiluncus spp (bacterial
vaginosis)
Genital Ulcers (Nonexudative
Infections)
Treponema pallidum
Syphilis
HSV-2 >> HSV-1
Herpes
Haemophilus ducreyi
Chancroid
Chlamydia trachomatis
Lymphogranuloma Venereum
Human papillomavirus (HPV)
Genital Warts (Condylomata acuminata)
Sexually Transmitted Systemic
Infections
HIV-1, HIV-2
AIDS
Polymicrobic : N.go, C.trach. anaerob
Pelvic Inflamatory Disease (PID)
Cancer (Neoplasia)
 1. Gonorrhoeae
General characteristics :

 oxidase-positive, gram-negative
diplococcus, kidney bean” morphologic
appearance
 epidemic, the highest incidence in the
most sexually active groups (age 15-25
years).
Neisseria gonorrhoeae
 Pathogenicity
Produces IgA-ase that degrades IgA1; this
antibody probably plays a key early role in
mucosal infections. (IgAase is also found
in Haemophilus and streptococcal
organisms).
Possesses a plasmid that codes for
penicillinase production.
Possesses pili, which are protein surface
fibrils that mediate attachment to the
mucosal epithelium.
 Pathogenicity
1. Pili undergo phase variation (on/off
switch of pili production). Nonpiliation
greatly reduces virulence.

2. Pili also exhibit antigenic variation and

have the capacity to produce millions
of variants, which is partly responsible
for the lack of protection against
subsequent infection.
 Pathogenicity
Possesses outer membrane proteins that form
porins (PI and PIII) and that determine clumping
-
(PII) or opacity. PII strains are isolated from
disseminated forms. Pili and PII play major roles
in adherence

Possesses endotoxin activity that damages

mucosal cells. Unlike most LPSs, N. gonorrhoeae
lacks lengthy O-antigenic side chains and is
termed lipo-oligosacharide (LOS)
 Clinical disease
results in mucous membrane infections,
primarily in the anterior urogenital tract.
is absent in 20% to 80% of infected women and
10% of infected men; these asymptomatic
carriers may transmit the bacteria to
consorts, causing symptomatic gonorrhea.
is compared with other sexually transmitted
diseases
repeated infection may cause scarring with
subsequent sterility in either gender and
may predispose women to ectopic pregnancy
 Clinical disease
 Reflects various types of infections including:
1. Urethritis in men is characterized by thick, yellow,
purulent exudate containing bacteria and numerous
neutrophils; frequent, painful urination; and
possibly an erythematous meatus. Complications :
epididymitis and prostatitis in males
2. Endocervicitis or urethritis in women is characterized
by a purulent vaginal discharge, frequent, painful
urination, and abdominal pain. Approximately 50% of
cases go undiagnosed. Complications : arthritis,
pelvic inflammatory disease, and sterility.
 Clinical disease
3. Rectal infections (prevalent in homosexual males),
characterized by painful defecation, discharge,
constipation, and proctitis.
4. Pharyngitis : characterized by purulent exudate, the mild
form mimics viral sore throat, whereas the severe form
mimics streptococcal sore throat.
5. Disseminated infection (bloodstream invasion) : infection
in which organisms initially localize in the skin, causing
dermatitis (a single maculo-papular, erythematous
lesion), spread to the joints, causing overt, painful
arthritis of the hands, wrists, elbows, and ankles.
6. Infant eye infection (ophthalmia neonatorum), which is
contracted during passage through the birth canal,
characterized by severe, bilateral purulent conjunctivitis,
may rapidly lead to blindness.
 Laboratory Diagnosis
1. Identification
a. Gram-negative, intracellular and extracellular
diplococci. Numerous neutrophils appear in purulent
exudate in men.
Because of endocervical localization, a characteristic Gram
stain of organisms is less likely in females.
b. Culture should be immediately placed on warm Thayer-
Martin chocolate agar in a candle jar.
c. Oxidase test is positive.
d. Organisms utilize glucose but not maltose.
e. Newer techniques involve immuno-fluorescence,
enzyme-linked immunosorbent assay (ELISA) on gene
probes on a clinical swab.
 Clinical Specimens
a. In women, both genital and rectal cultures
should be obtained.
b. If a speculum or anoscope is used,
lubricant should not be used because it
kills many organisms and reduces the
chance for a successful culture.
c. The organisms are labile, and specimens
should be plated immediately.
d. If disseminated gonorrhea is present,
blood and synovial fluid should be
cultured; culture of skin lesions is rarely
 Control
1. Treatment
a. Ceftriaxone should be given, followed by a
tetracycline to treat possible chlamydial
infection.
b. In approximately 50% of cases, pelvic
inflammatory disease is severe enough to
warrant hospitalization.
c. Pelvic inflammatory disease predisposes the
patient to repeated episodes caused by
other bacteria and to ectopic pregnancy.
 Control
2. Prevention
a. The patient's sexual partners should be
treated and condom use should
encouraged.
b. Asymptomatic patients should be identified
by culture and treated.
c. To prevent neonatal gonococcal conjunctivitis
topical silver nitrate or tetracycline should
be used; the antibiotic is preferred because
it also kills Chlamydia trachomatis, if
present.
2.Lymphogranuloma Venereum (LGV)
Chlamydia trachomatis infection is one
of the most common sexually transmitted
infections world wide
Occurring in men and women under the
age of 25.
This is most likely an underestimate, since
half of people with chlamydia likely have
gonorrhea too.
Chlamydia trachomatis
•Lymphogranuloma
• Serovars L1-L3 venereum

Trachoma
• Serovars A, B, Ba,C (hyperendemic blinding)
Inclusion conjunctivitis (newborn)
•Neonatal pneumonia
•Urethritis
• Serovars D-K •Cervicitis
•rs D-K •Pelvic inflammatory disease
•Association with cervical cancer
•Pneumonia (human
Chlamydia psittaci psittacosis, avian
chlamydiosis)
Chlamydia pneumoniae
(TWAR strain) •Pneumonia
CHLAMYDIA LIFE CYCLE
Once inside the endosome, the glycogen produced
causes the elementary body to "germinate" into the
vegetative form, the reticulate body.
This form divides by binary fission at approximately
2-3 hours per generation. It has an incubation
period of 7-21 days in the host.
It contains no cell wall and (when stained with
iodine) is detected as an inclusion in the cell. After
division, the reticulate body transforms back to the
elementary form and is released by the cell by
exocytosis.
One phagolysosome usually produces 100 – 1000
elementary bodies.
 Laboratorium Diagnosis

Diagnosis of C. trachomatis infection is

based on clinical symptoms that are
difficult to differentiate with Nesisseria
gonorrhoeae infection and other
aetiologic.

Laboratory examination is very useful to

confirm the definitive organisms.
Chlamydia trachomatis infection
 LABORATORY EXAMINATIONS
Collection of specimens
Chlamydia is an intracellular pathogen.
Obtain swab specimens containing
epithelial cells of cervix, rectum or urethra.
Urethra : Patient should not urinate within
1 hour prior to specimen collection. The
swab should be inserted 2 cm into the
urethra. Use firm pressure to scrape cells
from the mucosal surface. If possible
repeat with second swab.
 LABORATORY EXAMINATIONS
Cervix : Remove mucous/pus with a
swab, discard, and use firm and rotating
pressure to obtain specimen with another
swab. May be combined with a urethral
swab into same transport medium. This
combination of cervical and urethral
method is highly recommended.
Rectum : Sample anal crypts with a
swab. Avoid contamination with fecal
material.
 Clinical disease
1. Subtypes D-K
cause a sexually transmitted disease that may involve
an associated inclusion conjunctivitis.
are a prominent cause of nongonococcal urethritis
(men) and urethritis, cervicitis, salpingitis, pelvic
inflammatory disease (women)
produce a relatively high incidence of asymptomatic
or relatively inapparent infections.
can produce a self limiting inclusion cojunctivitis in
neonates delivered through an infected birth canal.
may cause neonatal pneumonia
 Clinical disease
2. Subtype Ll, L2, L3
causes a sexually transmitted disease
called lymphogranuloma venereum,
which is characterized by a suppurative
inguinal adenitis.
may cause lymphadenitis to progress
to lymphatic obstruction and rectal
strictures if the disease is untreated.
 DIAGNOSTIC TESTS
Detection of the bacterium can be
ccomplished using both non-culture and
culture tests :
1. Cytology - Examination of stained cell
scrapings for the presence of inclusion
bodies has been used for diagnosis using
Giemsa and iodine staining, but this
method is not as sensitive as other
methods.
 DIAGNOSTIC TESTS
2. Leukocyte esterase tests:
detects enzymes produced by leukocytes
containing the bacteria in urine
3. Culture - Culture is the most specific method
for diagnosis of C. trachomatis infections.
4. Antigen detection - Direct
immunofluorescence and ELISA kits that
detect the group specific LPS or strain-
specific outer membrane proteins are
available for diagnosis
 DIAGNOSTIC TESTS
5. Serology - Serological tests for diagnosis are of
limited value in adults, since the tests do not
distinguish between current and past infections.
Detection of high titer IgM antibodies is indicative
of a recent infection. Detection of IgM antibodies
in neonatal infection is useful.

6. Nucleic acid probes - Three new tests based on

nucleic acid probes are available, uses DNA
complementary to specific ribosomal RNA
sequences. These tests are sensitive and specific
and may replace culture as the method of choice.
 Control
1. Treatment is with doxycycline or
erythromycin.
2. Prevention is by diagnosing mothers of
infected neonates and urging standard
control measures (e.g., use of
condoms) to help prevent sexual
transmission.
 Lymphogranuloma Venereum (LGV)
Characterized by acute
inguinal lymphadenitis &
genital ulceration, it is also
called :
 Durand-Nicolas-Faver
disease
 Tropical or climate bubo
 Poradenitis
 Lymphopathia venereum
 Lymphogranuloma
inguinale
 3. Syphilis / Lues
General characteristics
is a corkscrew-shaped, motile organism with
unusual morphologic appearance of the outer
envelope, three axial filaments, a cytoplasmic
membrane-cell wall complex with endotoxin,
and a protoplasmic cylinder.
causes chronic, painless infections that may
last 30 to 40 years if untreated.
decreases in number as host defenses are
stimulated, causing disappearance of
symptoms; subsequently, organisms multiply
and symptoms reappear.
 Classification
1. Subspecies pallidum causes syphilis,
which is sexually transmitted,
epidemic worldwide, and may affect
any tissue.
 Pathogenicity
Immunosuppressive treponemal components
are responsible for the chronic nature of
syphilis and for subsequent emergence of
different stages.

Clinical disease-syphilis
1. Vascular involvement leads to endarteritis
and periarteritis, resulting in inhibited
blood supply and necrosis.
2. Lymphocyte and plasma cell inf'iltration
occurs at sites of infection.
The pathogenesis of syphilis varies considerably. It may
involve many tissues of the body and is generally
divided into three stages :
1. Primary - localized infection with erythema,
induration with a firm base (a hard chancre), and
ulceration
2. Secondary - disseminated infection with lesions in
almost all tissues; mucocutaneous rash; may recur if
untreated
3. Tertiary - aortitis and CNS problems may be fatal
In utero infection has severe manifestations, including
abortion, stillbirth, birth defects, or latent infection
(most common) with the snuffles (rhinitis) followed by
 Laboratory diagnosis
Clinical specimens
a. Lesion exudate should be obtained from a
pustule or an ulcer for darkfield microscopy.
b. The organism cannot be grown in vitro.
Identification
Syphilis is identified partly on the basis of
clinical manifestations.
Darkfield microscopy of lesion exudate may
demonstrate cork-screw-shaped spirochetes
(the organisms are too thin to identify by Gram
stain).
Serology. Two antibodies are produced in response
to T. pallidum infection:
(1) Nontreponemal (reaginic) antibodies (these are
not IgE)
- are nonspecific (positive in many related or chronic
diseases) but economical as a screening test.
- are identified by other screens: Venereal Disease
Research Laboratory (VDRL) test, rapid plasma
reagin (RPR) card test, or automated reagin test
(ART).
- titers are decreased in tertiary syphilis (even if
untreated). If treated, a positive reagin test after 1
year suggests persistent infection, reinfection, or a
false-positive result.
(2) Specific treponemal antibodies
- are more specific, but tests are costly and are
used only to confirm a positive reagin test.
- are screened for by fluorescent treponemal
antibody absorption (FTA-abs) test, T.
pallidum hemagglutination (TPHA) test, and
the rarely used T. pallidum immobilization
(TPI) test.
- titers remain positive in most people even
with proper treatment.
- biologic false-positive results may confuse the
diagnosis (positive serology in the absence of
treponemal disease).
 Control
1. Treatment
a. Long-acting penicillin should be given.
b. Jarisch-Herxheimer reaction immediately
after antibiotic therapy for secondary
syphilis involves intensification of
manifestations for 12 hours; this indicates
that penicillin is effective.
c. With treatment, reagin-based serologic tests
become negative 6 months after primary
syphilis and 12 months after secondary
syphilis; beyond the secondary stage, the
patient may remain seropositive for years.
2. Prevention
a. Use of a condom minimizes
transmission.
b. All sexual contacts should be
treated prophylactically with
penicillin.
c. In pregnant patients, serologic
syphilis tests should be
performed during the first and
third trimesters.
 4. Chancroid
Chancroid or soft chancre
disease is an acute
sexually transmitted
disease characterized by
genital ulceration and
suppuration
Haemophylus ducreyi
/Ducrey's bacillus) is a
Gram(-) rod which grows in
chains.
 Pathology and pathogenesis
The organism enters the body through
skin abrasions.
It induces a papule or vesicle which
ulcerates.
There is a dense inflammatory exudate
with PMNs but not mononuclear cells.
Incubation period of 1-14 days after
exposure before you get the
development of the characteristic lesion,
the soft chancre.
 Clinical manifestations
 Chancre development begins as a small
inflammatory papule.
 The lesion is a true ulcer.
 In contrast to the syphilis chancre, the chancroid
is extremely painful.
 Accompanying chancroid development is an
acute, painful inflammatory inguinal lymph-
adenopathy in > 50% of cases.
The chancroid
lacks induration
and is referred to
as a soft chancre.

Initially the lesion

is typically
solitary but by
autoinoculation
multiple lesions
develop.
 5. Granuloma inguinale
Granuloma inguinale (also called lupoid
ulceration granuloma of the pudenda and
granuloma contagiosa) is a chronic, indolent,
ulcerative, granulomatous disease of the skin
and lymphatics.

Calymmatobacterium granulomatis : Gram -

rod with characteristic bipolar staining so they
have a safety pin-like appearance in stained
tissue preparation : Donovan bodies.
 Manifestations
 Genital lesions are present in 90% of infected
patients and in 80% of these there is no other
area of involvement.
 Initially the lesions are papules that tend to
ulcerate slowly.
 The ulcerated lesions are irregular in shape
with a rolled border on a beefy red,
cobblestone base
 Patients develop subcutaneous
granulomas in the inguinal regions; they do
not involve the lymph nodes usually, so we call
them pseudo-buboes.
 Pathology and pathogenesis
 Theorganism gains entry by direct
inoculation through skin abrasions or
mucous membranes

 Oneor more indurated papules form which

progress to characteristic ulceration.

 Themost important sign is the presence of

mononuclear cells with intra cytoplasmic
vacuoles packed with the bacteria or
Donovan bodies as they are called.
 Therapy
In order of preference :
Trimethoprim-sulfamethoxazole one double-
strength tablet orally twice a day for a minimum of 3
weeks, OR
Doxycycline 100 mg orally twice a day for a
minimum of 3 weeks.
Alternative therapy
Ciprofloxacin 750 mg orally twice a day for a
minimum of 3 weeks, OR
Erythromycin base 500 mg orally four times a day
for a minimum of 3 weeks.
Follow-up weekly AND Check sex partners
 KEY CONCEPTS HIV
 Preferentially binds to the CD4 receptor
found on helper T cells & monocytes; the
destruction of these cells ultimately disables
the immune system & makes the infected
individual vulnerable to opportunistic
infections
 Transmitted through sexual contact, IV drug
use, vertically (mother to child)
 Display antigenic variation
 Has a long latency period (average 10 years)
 Can currently be managed with antiviral
drugs but is otherwise nearly 100% fatal
 PATHOGENESIS & PATHOLOGY
Stages :
Primary infection
Dissemination of virus to lymphoid
organs
Clinical latency
Elevated HIV expression
Clinical disease
Death
The duration between primary infection &
progression to clinical disease ± 10 years
Death usually 3 years after onset of clinical
INTERPRETATION OF LABORATORY
EXAMINATION

1. Positive HIV infection :

 patient sera up to 15 months of age, HIV +,
even mother has no HIV
 patient sera < 15 months of age, HIV +,
mother HIV +, lymphocyte count 
 p24 Ag +
 HIV culture +, Ag +, RT-ase enzyme +, probe +
 Positive test with specific tests
INTERPRETATION OF LABORATORY
EXAMINATION

2. Negative HIV :
screening & confirmation tests –

3. Inconclusive :
 Screening test for HIV +,
confirmation, Ag, & culture are
negative
 Baby < 15 month of age HIV -, mother
HIV +
 HERPES VIRUSES
TRANSMISSION OF HUMAN HERPES VIRUSES

VIRUS MEANS OF PORTAL OF ENTRY INITIAL

TRANSMISSION TARGET CELLS

HSV-1 Direct contact Mucous membrane, skin Epithelial

HSV-2 Direct contact Mucous membrane, skin Epithelial

 HERPES SIMPLEX VIRUS

 Sangat tersebar luas dlm populasi

 Memperlihatkan host yg luas, mampu
bereplikasi dlm banyak tipe sel
 Tumbuh dgn cepat dan sifat cytolytic yg
tinggi
 Bertanggungjawab pd penyakit-penyakit :
 gingivostomatitis
 keratoconjunctivitis
 encephalits
 genital herpes
 infections of newborn
 Seringkali latent dlm sel syaraf
 HERPES SIMPLEX VIRUS

TRANSMISI
Kedua virus berbeda dalam cara
transmisinya :
 HSV-1 disebarkan mel. kontak,
biasanya melibatkan saliva yg
terinfeksi
 HSV-2 ditransmisikan mel. hubungan
seksual atau dari ibu yang terinfeksi
pada genitalnya ke bayinya
 HERPES SIMPLEX VIRUS

INFECTIONS ASSOCIATED WITH HERPES SIMPLEX VIRUS

Infection Predominant Frequency Age Usual Recurrence

virus type group outcome

Genital herpes 2>1 Common Adolescence, Resolution Yes

adults
Neonatal herpes 2 > 1 Very rare 0 – 4 weeks Developmental No
impairment
 HERPES SIMPLEX VIRUS
CLINICAL FINDINGS
Vesicular eruption at the skin or mucous
membrane
Incubation period is short :
3 – 5 days, with a range of 2 – 12 days
Clinical manifestation 2 categories
Primary infection
Reactivation
HSV-1 : oropharyngeal area
HSV-2 “ genital
 HERPES SIMPLEX VIRUS

CLINICAL FINDINGS
RECURRENT INFECTION

 Genital herpes : common &

tend to be mild, a limited
number of vesicles, heal in
10 days
 HERPES SIMPLEX VIRUS

Reactivation
Provocation :
 Common cold
 UV
○ Underlying disease
 Stress
- Hormonal (menstrual cycle)
HSV-2 : Oncogenic virus Ca-cervix & vulva
transformation of cell culture
inoculation of animal tumor
 VIRUS TUMOR DNA

1. Papovaviridae
Papova : Papilloma, Polyoma dan Simian Vacuolating

Suatu virus telanjang dengan genom DNA untai ganda

banyak di alam, menyerang manusia dan hewan.

Virus Papilloma Virus Polyoma

 Ø nukleokapsid 55 nm 45 nm
 genom >, pada salah satu pada kedua rantai DNA
rantai DNA
 hospes seluler : epitel per- mll saluran napas/cerna
mukaan, menimbulkan --> masuk aliran darah
kelainan pd port d’entry --> ke organ-organ dalam :
hati, ginjal, otak.
 VIRUS PAPILLOMA

HPV : Human Papilloma Virus

 > 60 tipe v msg2 tipe memp.cara
predileksi sndr
 Bereplikasi dlm inti sel hospes, Virus
Papilloma sulit dibiak dalam media
buatan
 Menyerang sel epitel gepeng kulit dan
mukosa, tipe Virusnya berbeda.
 HPV : Human Papilloma Virus

 Bagaimana proses karsinogenesis oleh Virus

Papilloma  ???
 Faktor lain :
Kebiasaan merokok & karsinogen kimia
Radiasi sinar gelombang pendek
Steroid
Reaksi radang lokal yang berkepanjangan
Infeksi setempat yang mengubah ekspresi
gen sel dan virus.
HPV : Human Papilloma Virus
 Veruca vulgaris (common warts) tipe
2,4,27,29,54.
Condilomalata (anal & genital warts)
* Condiloma acuminata tipe 6, 11, 54.

Sebagian besar Veruka bersifat jinak, dan

tidak berubah  ganas.

PENULARAN :
Kontak kulit dengan kulit
Hubungan kelamin (condiloma
acuminata)
 Hepadnaviridae
Virus Hepatitis B
Genom DNA untai ganda (panjang) dan DNA
untai tunggal (pendek) penyebab Ca
hepatoseluler.

Infeksi Hepatitis B khronis terdiri dari 2

tipe:
1. HBsAg (+) tp HBeAg (-) : taa disfungsi
hati
2. HBsAg dan Hbe Ag (+) : terjadi kerusakan
hati ----> dapat berkembang  Cirrhosis
hepatitis ----> Cahepatis
HBV Morphology

Structure & antigen complex

3 shapes in serum
. Dane particles : Ø 42 nm
. Spherical particles : Ø 22 nm
. Filament particles : Ø 22 nm
Genome ds DNA polimerase 3200 bp
Spherical
Molecular weight 2 x 106 kd
Antigen structure :

1. HBsAg Anti-HBs

2. HBcAg Anti-HBc

3. HBeAg Anti-HBe
MODE OF TRANSMISSION

- Parenteral

- Mucosal (per oral & sexual

contact)

- Vertically from mother to

baby
 SYSTEMIC MYCOSES
CANDIDIASIS = Candidosis
 acute / chronic fungal infections, involving, the mouth,
vagina, skin nails, bronchi / lung, alimentary tract,
urinary tract, blood steam and less commonly, the heart
or meningen
 are caused by Candida albicans or other species
 are predisposed by : extremes of age, wasting, &
nutritional disease, excessive moisture, pregnancy,
diabetes, long-term antibiotics, & steroid use, indwelling
catheter, immunosupressed & AIDS
 are generally treated with imidazoles, polyenes or both
 CANDIDIASIS
Candida albicans :
 is part of the normal flora of the skin, mucous
membranes & GI tract along with other Candida
sp.
 normal colonization must be distinguised from
infection
 form elongated “budding forms” called
pseudohyphae, which are often seen in clinical
material along with true hyphae, blastoconidia &
yaest cells
 CANDIDIASIS
Clinical features : Vulvovaginitis
 is a yeast infection of the vagina; manifest with
a thick yellow-white discharge, a burning
sensation, curd-like patches on the vaginal
mucosa & inflamation of perineum
 is predisposed by diabetes, antibiotic therapy,
oral contraceptive use & pregnancy
 may be trasmitted to sexual partner as balanitis
Terima kasih