INFECTIONS OCCURING IN

REPRODUCTION ORGANS

EFRIDA WARGANEGARA
I. SEXUALLY TRANSMITTED
(VENEREAL) DISEASES

II. OBSTETRIC AND

PERINATAL INFECTIONS
 SEXUALLY TRANSMITTED
(VENEREAL) DISEASES
 Sexually Transmitted Diseases (STD) / Venerial Diseases (VD) : are
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, these range from microscopic viruses (HIV) to visible
insect (pubic louse)
 STD usually result from having vagina, oral and anal sex with an
infected partner, but occasionally they may be transmitted by
kissing or close body contact
 Agents of some STD may be transmitted through food and water or
blood transfusion, contaminated medical instruments, or needles use
by injecting drug users
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
 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
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)
Cervical carcinoma HPV
Kaposi Sarcoma Human Herpes Virus type 8
 Infectious Agents of STD
1. Neisseria gonorrhoeae
2. Chlamydia trachomatis
3. Treponema pallidum
4. Hemophilus ducreyi
5. Ureaplasma urealyticum
6. Human Imunodefeciency Virus (HIV)
7. Human Papilloma Virus (HPV)
8. Herpes Simpleks Virus type – 2
9. Molluscum contagiosum
10. Hepatitis B dan C
11. Candida albicans
HIV - AIDS
The HIV  has become an important challenge to
the medical community since the manifestation of
infection by the virus were first discovered in
1979.
Infectionby HIV leads to progressive
deterioration of the immune system
This deterioration leads to the final stage of HIV
diseases called AIDS
To date AIDS is an incurable condition and no
vaccine is available
 KEY CONCEPTS
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
 CLASSIFICATION
Subfamily Disease caused Natural hosts
Oncovirinae
HTLV-I Adult T-cell leukemia, Human
lymphoma, tropical
spastic paraparesis
HTLV-II Hairy cell leukemia Human
Spumavirinae Inapparent Primates & other
persistent infection animals
Lentivirinae
HIV-1 Immunodeficiency Human
HIV-2 Immunodeficiency Human & primates
Monkey
SIV Immunodeficiency
PROPERTIES OF HIV
The human AIDS virus are not
homogenous, most are variants of
HIV-1, virus HIV-2 (West Africa,
much less virulent)
Based on env gene sequences
9 subtypes of HIV-1 A – I
5 subtypes of HIV-2 A– E
 PROPERTIES OF HIV
Virion : spherical, 80 – 100 nm, cylindric
core
Genome : SS-RNA, linear, positive sense, 9 – 10
kb
Proteins : envelope glycoprotein, reverse
transcriptase enzyme contained inside virions,
protease required for production of infectious virus
Envelope : present
Replication : reverse transcriptase makes DNA copy
from from genomic RNA; provirus DNA is template
for viral RNA
Maturation : particles bud from plasma membrane
STRUCTURE OF HIV
 STRUCTURE OF HIV
The virus contains the three genes required for
a replication
 gag : encodes core protein (group-specific
antigens
 pol : encodes  reverse transcriptase enzyme
(polymease)
 env : encodes  glycoproteins that form
projections on the envelope of the particle
Up to six additional genes regulate viral
expression & important in disease
pathogenesis in vivo.
 STRUCTURE OF HIV
 Additional genes :
tat or tax : transactivating regulatory gene encodes
a nonstructural proteins that alters the transcription
or translational efficiency of other viral gene
rev : regulator of expression of virion
 gp 120 : responsible  virus attachment
to the CD4 molecule and coreceptors &
carries the major antigenic determinants that
elicit neutralizing Abs
 gp 41 : contain transmembrane domain that
anchors the glycoprotein in the viral envelope
and a fusion domain that facilitate viral
penetration into target cells
VIRAL REPLICATION
 DISINFECTION & INACTIVATION

 HIV completely inactivated by treatment for 10

minutes at room temperature with :
 50 % ethanol - 35 % isopropanol
 0,5 % Lysol - 0,5 % paraformaldehyde
 0,3 % hydrogen peroxide

 Also inactivated by extremes pH : pH 1.0 & 13.0

 HIV inactivated by heating at 560C for 10 minutes
 CELL TROPISM
IN VITRO IN VIVO
 T lymphocyte, CD4+ T lymphocyte, CD4+
 Monocyte/ Monocyte/
macrophage macrophage
 Microglia Epithelial Langerhans
 Precursor CD 34+ cells
cells Dendritic cells
 Monocytic & T-cell Endothelial cells of
lines the brain
 Glioma & neuro- Microglia, astroglia,
blastoma cell lines oligodendroglia
 Tumor cell lines Cells of retina, cervix
and colon
IMMUNODEFICIENCY PROCESS
MODE OF TRANSMISSION
 Parenteral (IV, drug use)
 Mucosal (sexual contact)
 Vertical (mother to child)

Free HIV HIV in CD4+ T cells

regional lymph nodes

Cellular IR Humoral IR
 Limphopenia
 CD4+ cells
 Free virus & p24 in blood
 Number of infected CD4

 Virus rapid replication

with control of IR

2 – 4 weeks

Totallymphocyte CD8
Antibody + : 2 – 3 weeks months
 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
syndrome
PATHOGENESIS & PATHOLOGY
Following primary infection,
viral replication occurs &
viremia detectable for about 8 –
12 weeks
Virus is widely disseminated
throughout the body & the
lymphoid organs become
seeded
PATHOGENESIS & PATHOLOGY
The period of clinical latency may last
for as long as 10 years. During this
period, there is a high level of ongoing
viral replication, estimated that 10
billion HIV particles are produced &
destroyed each day.
The half life of virus in plasma is about
6 hours, and the virus life cycle (from
the time of infection of cells to the
production of new progeny that infect
the next cell) averages 2.6 days
 CLINICAL FINDINGS
AIDS is characterized by a pronounced
suppression of the immune system & the
development of unusual neoplasms
(especially Kaposi’s sarcoma) or a wide
variety of severe opportunistic infections
Plasma viral load :
the amount of HIV in the blood (viral
load) is of significant prognostic value.
Plasma HIV RNA levels can be
determined using a variety of
commercially available assays.
CLINICAL CATEGORIES OF HIV INFECTION
IN PERSONS > 13 YEARS OF AGE
1. Category A :
Asymptomatic
Persistent generalized adenopathy
Symptomatic, acute (primary) HIV
infection
2. Category B :
Some conditions are diagnosed
3. Category C :
Any of some conditions are diagnosed
CDC DEFINITION OF AIDS
Clinical category
CD4+ T-cells AB C

500/l A1B1 C1

200 – 499/l A2B2 C2

<200/l A3B3 C3

AIDS is diagnosed if the patient meets criteria for

category A3, B3, C1, C2, or C3
OPPORTUNISTIC INFECTIONS

 PROTOZOA  BACTERIA
Toxoplasma gondii Mycobacterium avium- intracellulare
Isospora belli Mycobacterium tuberculosis
Listeria monocytogenes
Cryptosporidium sp.
Nocardia asteroides
Salmonella sp.
 FUNGI Streptococcus sp.
Candida albicans
Cryptococcus  VIRUS
neoformans Cytomegalovirus
Coccidioides immitis Herpes simplex virus
Histoplasma Varicella-zoster virus
capsulatum Adenovirus
Pneumocystis carinii JC human papovavirus
Hepatitis B virus
 LABORATORY DIAGNOSIS

Evidence of HIV infection :

1. Virus isolation
Cultured from lymphocyte in peripheral blood or
other specimens, but time consuming
2. Serologic determination of antiviral Abs
ELISA, antibody repeated
Confirmation : immunofluorescence &
radioimmunoprecipitation,
Western blot : at least 2 bands of p24, gp41 or
gp120/gp 160 should be present
3. Measurement of viral nucleic acid or Ag
RT-PCR
LABORATORY DIAGNOSIS

Examination of immunity status

- CD4, CD8
- Hematology

Examination of opportunistic infection /

malignancy
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 +
ANTIRETROVIRUS DRUG FOR HIV
INFECTION
 NNRTI (NON-NUCLEOSIDE ANALOG REVERSE
TRANSCRIPTASE INHIBITOR
* Nevirapine
* Delavirdine mesylate

 NRTI(NUCLEOSIDE ANALOG REVERSE

TRANSCRIPATSE INHIBITOR)
* Didanosine (ddI) * Lamivudine (3TC)
* Zalzitabine (ddC) * Stavudine (d4T)
* Zidovudine (AZT : Azydothymidine

 PROTEASE INHIBITOR
* Indinavir * Ritonavir
* Nelfinavir mesylate * Saquinavir
 HERPES VIRUSES
KEY CONCEPS
 Mengandung bbp patogen yg paling penting pd
manusia
 Dikharakteristikkan dgn adanya infeksi latent
yg diikuti infeksi primer
 Masa latent menghasilkan gejala-gejala
rekurent yang tetap persisten sepanjang
kehidupan individu yang terinfeksi
 Adalah“ubiquitous” pada manusia, misal hampir
semua individu telah terinfeksi dengan HSV
type-1
 HERPES VIRUSES
KEY CONCEPS
 Kebanyakan infeksi adalah asymptomatik
 Secara klinik :
Memperlihatkan suatu spektrum dr penyakit
Bbp memp. host yg luas, sedangkan yg lain
memp. host yg sempit
Kemampuannya utk tetap sbg infeksi yg
persisten sepanjang hidup dan mengalami
reaktivasi secara periodeik
 Dapat diobati dgn antiviral, namun antiviral tak
dpt mencegah rekurent
 Terakhir, vaksin vericella telah tersedia
 HERPES VIRUSES
TRANSMISSION OF HUMAN HERPES VIRUSES

VIRUS MEANS OF PORTAL OF ENTRY INITIAL

TRANSMISSION TARGET CELLS

HSV-1 Direct contact Mucous membrane, skinEpithelial

HSV-2 Direct contact Mucous membrane, skinEpithelial

 HERPES VIRUSES
VIRAL REPLICATION
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
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
HERPES SIMPLEX
SIMPLEX VIRUS
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
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS

PATHOGENESIS :
PRIMARY INFECTION LATENT INFECTION
Oropharyngeal HSV-1 infections Virus resides in latently infected
results in latent infection in the ganglia in a nonreplicating
trigeminal ganglia state, only a very few viral
genes are expressed
Genital HSV-2 Viral persistence in
infection lead to latently infected
latently infected ganglia lasts for
sacral ganglia the lifetime
Primary infections : usually mild, More than 80% of the human
in fact most are asymptomatic population harbor HSV-1 in
(85 – 90%) latent form, only a small
portion recurrence
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
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
HERPES SIMPLEX
SIMPLEX VIRUS
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
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
CLINICAL FINDINGS
CLINICAL HSV-1 HSV-2
Primary infection
Primary
Recurrent or recurrent infection
Gingivostomatitis + -
Cold sores, herpes
Cutaneous fever blisters + -
Pharyngotonsilitis + -
Keratitis
Skin above the waist
Keratoconjunctivitis + ++ - - -
Skin below
Neonatal the waist
infections - ± + +
Hands or arms + +
Herpetic whitlow + +
Eczema herpeticum + -

Genital herpes ± +
Herpes encephalitis + -
Herpes meningitis + +
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
CLINICAL FINDINGS
RECURRENT INFECTION
 Genital herpes : common &
tend to be mild, a limited
number of vesicles, heal in 10
days
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
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
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
IMMUNITY

Many newborns acquire passively transferred

maternal Abs, lost during 6 months, not totally
protected against infection of newborns
During primary infections, IgM Abs appear
transiently, and followed by IgG & IgA that persist for
long period
Abs do not prevent reinfection or reactivation of
latent virus, but maybe subsequent disease
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
LABORATORY DIAGNOSIS
ISOLATION & IDENTIFICATION
Specimens : swab or vesicle fluid
HSV has a wide host range ------------- many cell culture system are
susceptible
 Appearance of CPE in cell cultures in 2 – 3 days
 identified by Nt test or immunofluorescence staining
 Hybridization using DNA probes & DNA amplification

• SEROLOGY
Abs appear in 4 – 7 days after infection, reach a peak after 2
– 4 weeks
can be measured by Nt, CF, ELISA, RIA, IF
 HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
TREATMENT

Inhibitors of viral DNA synthesis

The drugs inhibits virus replication &
suppress clinical manifestation
HSV remain latent in sensory ganglia
Acyclovir (acycloguanosine) : topical,
intravenous, oral
Vidarabine : more toxic
 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.
Kelainan bersifat lokal, ditandai oleh
perubahan morfologi & hiperplasia akibat
percepatan proliferasia dan terhambatnya
degeneralisasi sel.
Sifat kelainan :
a) tetap jinak;
b) displastik (mitosis tidak terkontrol &
perubahan kromosom;
c) Ca, ditandai oleh invasi sel ke
jaringan sekitar atau metastase jauh
ke organ lain.
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.

Diagnosis Laboratorium
1. Deteksi Virion dari lesi
Dengan mikroskop elektron
Papilloma laring dan genital ----> sukar
2. Deteksi Antigen Virion pada jaringan lesi.
3. Isolasi dan Identifikasi virus hanya untuk beberapa tipe
virus Papilloma.
4. Pem. Histopatologi
Adanya kelainan morfologi sel akibat infeksi virus
Papilloma.
Kadang-kadang ditemukan sel dengan banyak inti.
5. Deteksi gen virus
Kepekaan : tinggi ---> tidak tergantung ada / tidak virion
atau Ag dalam sel.
 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)
PENGOBATAN

Tergantung : jenis, besar, lokasi kelainan.

 Ekstirpasi / Insisi lesi

 Kauterisasi atau Cryosurgery
 Lesi jinak : hindari radiasi, oleh karena diduga
merangsang rekombinasi genetik antara fragmen
gen virus dan gen sel sehingga terjadi konversi lesi
dari jinak menjadi ganas.
 Khemoterapi
Podophyllin  untuk condiloma acuminata
Interferon 
Nitrogen cair  untuk Veruka pada kulit
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
 Hepatitis B virus particle

Virion 42 nm Nucleus Lysis nucleus

HBsAg / Dane virion 28 nm
virion (HBeAg)
particle HBcAg
Antigen structure :

1. HBsAg Anti-HBs

2. HBcAg Anti-HBc

3. HBeAg Anti-HBe
STABILITY
 Temperature – 20oC more than
20 years
 Dry, 25oC stay for 1 week
 Temperature 100oC, 1 minute
 pH 2,4 for 6 hours
 Sodium hypochlorite 5% for 3
minutes
Viral replication :

Attachment – Uncoating – DNA

within nucleus (transcription) –
mRNA (translation) – RNA
(reverse transcription) – cDNA –
re enter to previous cycle
 Attachment

Reenter cycle

Uncoating

Host DNA repair AAA Positive-

AAA
AAA
strand DNA
cccDNA synthesis
mRNA
Nucleus

Translation

Encapsidation
Negative-strand
DNA
Cytoplasm
3.5 kb RNA synthesis

HBV replication cycle

MODE OF TRANSMISSION
- Parenteral

- Mucosal (per oral & sexual

contact)

- Vertically from mother to

baby
Laboratory examination

Isolation : cell culture difficult

Diagnosis :
Serology (Ag – Ab)
Transaminase enzyme (LFT)
Histology (biopsy)
PCR (molecular)
Electron Microscopy (virus particle)
Leucopenia during pre jaundice phase
 Prodrome,
Convalescence
Acute diseases
Incubation Early
period
Important HBsAg HBsAg IgM-anti HBc Anti HBs
diagnosis IgG anti-HBc
tests
1 2 3 4 5 6 7 8 9

Relative
concentration
Anti-HBc
of reactants

HBsAg Anti HBs

HBeAg Anti-HBe
Level of
detectio
n after
Month
exposure 1 2 3 4 5 6 7 8
ALT
Symptoms

Clinical and serologic events occurring in patient with acute

hepatitis B infection
 SEROLOGICAL INTERPRETATION OF HBV
INFECTION
Results Interpretation
HBsAg (+) Hepatitis B infection active, acute/ chronic
Anti-HBs (+) Protection to reinfection (immunity)
HBsAg (-) (+) after > 16 weeks, persist for years
Anti-HBc (+) Might be HBV active infection
Anti-HBs (-) Should be confirm IgM anti-HBc,  3 months
Total anti-HBc persist 5-6 years
HBeAg (+) Infectious active hepatitis, acute / chroni
HBsAg (+) Potential infectious
Anti-HBe (+) Non infectious blood
Carrier state
 Prevaccination screening hepatitis B
HBsAg (+) HBsAg (-) HBsAg (-) HBsAg (-) HBsAg (-)
Anti-HBs (-) Anti-HBs (-) Anti-HBs (+) Anti-HBs (+) Anti-HBs (-)
Anti-HBc (-/+) Anti-HBc (+) Anti-HBc (+/-) Anti-HBc (+/-) Anti-HBc (-)
Titer > 10 mU/ml Titer < 10 mU/ml

No Postpone No Booster Vaccination

Vaccination vaccination vaccination

LFT Check Measure titer Measure titer Measure titer

examination anti-HBs anti-HBs anti-HBs anti-HBs
3-6 months
Molluscum contagiosum virus
Molluscum contagiosum is a specifically human
disease of worldwide distribution.
The incubation period varies from 1 week to 6 months.
The lesion begins as a small papule and gradually
grows into a discrete, waxy, smooth, dome-shaped,
pearly or flesh-coloured nodule. Usually 1-20
lesions but occasionally they may be present in
hundreds.
In children, the lesions are found on the trunk and the
proximal extremities.
In adults they tend to occur on the trunk, pubic area
and thighs. Individual lesions persist for about 2
months, but the disease usually lasts 6 to 9 months.
Constitutional disturbance is rare.
Molluscum contagiosum virus
The disease occurs world-wide and is spread by direct
contact or fomites. In general it tends to occur in
children. The disease by may transmitted from skin to
skin after sexual intercourse.
A diagnosis can usually be made on clinical appearance
alone. The diagnosis can be supported by EM. Unlike
other poxviruses, molluscum have not been
demonstrated to grow in cell culture.
Infection is usually benign and painless, with
spontaneous recovery in most cases.
Where treatment is required for cosmetic reasons,
various procedures are available such as curretage,
cryotherapy with liquid nitrogen, silver nitrate etc.
which are routinely used for the removal of warts.
SYMPTOMS
Molluscum contagiosum is a superficial skin
infection. 
The virus invades the skin causing the
appearance of firm, flesh-colored, doughnut-
shaped bumps, about 2-5 mm in diameter. 
Their sunken centers contain a white, curdy-
type material.  The bumps can occur almost
anywhere on the body including the buttocks
CAUSE
Molluscum contagiosum is caused by a virus
belonging to the poxvirus family. 
Close physical contact is usually necessary for
transmission; indirect transmission from shared
towels, swimming pools, etc., may also be
responsible for infection. 
The incubation period varies from several
weeks to several months.  Shaving or
scratching may cause the infection to spread.
 
 COMPLICATIONS

If scratched, the bumps can become infected

with bacteria.
 
 DIAGNOSIS

The diagnosis is based on the typical

appearance of the bumps. 
No diagnostic test for this virus is available.
 
 TREATMENT
Avoid shaving infected areas. 
Treatment is done for aesthetic reasons and to prevent
spread of the virus. 
The goal of treatment is to remove the soft center, after
which the bump goes away. 
Your health care provider may use a curette (sharp,
spoon-shaped instrument) to remove the centers. 
Freezing the lesion with liquid nitrogen or nitrous oxide
is an alternative treatment.
 
 RISKS OF TREATMENT
There is a slight risk of minimal scarring. 
Observe for signs of infection that include redness,
swelling, pus-like drainage, or increased soreness at
the site.
 
TERIMA KASIH