GENITAL DISCHARGE SYNDROME Universitas Lambung Mangkurat

PENYAKIT –PENYAKIT YANG DAPAT DITULARKAN MELALUI INFEKSI

MENULAR SEKSUAL

Sifilis Kandidosis /Kandidiasis vulvovaginal

Gonore Kondiloma Akuminata
Uretritis non spesifik Hepatitis-B
Trikomoniasis Sitomegalovirus
Chancroid Epstein-Barr Virus Infeksi
Lymfogranuloma venereum Pedikulosis pubis
Donovanosis Scabies
Herpes genital
Intestinal Protozoa
Vaginosis Bakterial
HIV
Molluscum kontangiosum
SINDROM IMS
Duh Uretra pada laki
Duh Vagina
Ulkus Genital
Bubo inguinal
Pembengkakkan skrotum
Nyeri perut bawah pada wanita
Tumbuhan (vegetasi) Genital
Konjungtivitis pada neonatus
SINDROMA DISCHARGE URETHRA
•Infeksi N. gonorrhoe & C. trachomatis  penyebab terbanyak
•Mudah dikenal baik oleh penderita maupun klinisi
•Dikenal sebagai Uretritis menular seksual
•Ditandai dengan adanya eksudat dlm uretra yg akan keluar dari mulut uretra
sebagai discharge uretral “kencing nanah”
•Neissseria gonorrhoeae :
•Gram negative, bentuk spt biji kopi, dapat resistensi penisilin, x suhu>39
URETHRITIS GONORRHEA
EPIDEMIOLOGI
Nama Gonorrhoeae berasal dari bahasa Greek terdiri dari kata gonos (seed) dan rhoia
(flow) menggambarkan satu keadaan ”semen mengalir (keluar) dari organ vital laki-laki
tanpa ereksi”.
Ada hubungan, umur, sex, race, sosioekonomi status, marital status, urban tendence, level
education, risk factor several behavior.
Highest rate terjadi pada tenager kurang educated dan belum kawin.
Wanita 50% : kemungkinan kena infeksi jika sexual kontak dengan
laki-laki yang terinfeksi.
Laki-laki 20% : kemungkinan kena infeksi jika melakukan sexual
kontak dengan wanita terinfeksi.
Asymptomatic infection selalu pada wanita secara sistemik dan ascenderen. Infeksi
vertical bisa terjadi dari ibu ke bayi waktu melahirkan dan manifest pada mata
Opthalmia Neonatorum.
Penyebab :
- “Neisseria Gonorrhoeae.
- Tidak memproduksi exotoxin.
- Inflamatory responses
- Persistent tanpa pengobatan dapat menyebabkan Chronic Inflamation dan Fibrosis
- Infection site of entry via vagina dan urehtral mucosa dari penis.
- Tetapi bisa juga di kerongkongan dan rectum tentang cara mereka melakukan
kontak sexual.
- Bakteri punya adhesive mechanism dan cepat membiak, menyebar ke cervix pada
wanita dan urethra pada laki-laki.
OPTHALMIA NEONATORUM
URETHRITIS GONORREA
Symptomp terjadi 2-7(3-14) hari setelah Peritoneal spreading menyebabkan
infeksi dengan karakteristik : perihepatic inflamation disebut Fitz-
 Laki-laki : Urethral discharge, sakit waktu Hugh-Curtis syndrome.
kencing (dysuria)
 Wanita : Vaginal discharge. GO infection pada kerongkongan terasa
kering (sakit menular).
50%  symptom hanya ringan bahkan
asymptomatic. Infection pada rectum bisa
menyebabkan purulent
Tanpa disadari bisa terjadi konplikasi discharge(proctitis)
pada wanita.
 Pelvic Inflamatory Disease (PID)
 Chronic Pelvic Pain
 Infertility akibat dari kerusakan (damage)
fallopian tubes.
FITZ HUGH CURTIZ SYNDROME
ORAL GO
GONORRHEA
Pria
Primary site: urethra
Subjektif
 rasa gatal, panas disekitar OUE, nyeri kencing
Objektif
 Duh tubuh uretra, kental, putih atau
kuning,kadang-kadang mukoid atau
mukopurulen, eritema atau edema pada meatus
 Terkadang dijumpai pembesaran kel limfe
inguinal bilateral
Komplikasi: epididymitis, infertilitas
Wanita
Primary site: endocervix
Sering asimtomatik, bila ada duh
tubuh serviks purulen atau
mukopurulen, kadang-kadang
disertai eksudat purulen dari uretra
atau kelenjar Bartholin.
Komplikasi: PID, ectopic pregnancy,
infertilitas
PEMERIKSAAN LABORATORIUM
Bahan
Specimen = sekret dari urethra, prostat, vagina, rectum, orofaring, serviks, kelenjer
Bartholini (Bartholinitis). Neonatus Oftalmia  sekret konjungtiva

A. Cara langsung:
 Dengan Ose (Sengkelit)  direct smear – Gram pada object glass
 Hasil : diplococcus gram negatif dalam/di luar PMN.
 Cara ini sensitivitas dan specificitas tinggi > 85%
NEISSERIA GONORREA
Diplokokkus gram negatif, seperti biji kopi
Intra & ekstraseluler
Tidak tahan lama diudara bebas, cepat mati pada keadaan kering, tidak tahan t。> 39。C,
tidak tahan desinfektan
Gerak (-), spora (-)
4 tipetipe 1 & 2 pili (+)virulensi
tipe 3 & 4 pili (-)non virulensi
~ plasmid gen resisten penisilinase
Betalaktamase Hidrolisis penisilin
Endotoksin, protease memecah IgA
PEMERIKSAAN LABORATORIUM
B. Cara Kultur
Neisseria Gonore (Neisser 1879)
1882 3 spesies : N. mengitis, N. catarrhalis, N. pharingitis Sicca  ke 4
ini dibedakan dengan cara kultur, dilanjutkan dengan tes fermentasi

Kultur Agar darah, thayer martin,NYCM

Media transport  Stuart, carry blair, Amies
Media transgrow  TM + Timetropim
PEMERIKSAAN LABORATORIUM
 Media transpor : Media stuart
tahan 96 jam  Media Transgrow, N. gonorrhoeae dan N. meningitidis
 Media Pertumbuhan :
Media Thayer-Martin : mengandung vancomysin untuk menekan pertumbuhan bakteri
positif, nistatin (jamur)
Modifikasi Thayer-Martin : ditambah dengan trimetoprim untuk mencegah
pertumbuhan kuman Proteus spp.
Agar coklat Mc Leod : tidak bagus oleh karena dapat ditumbuhi kuman selain
gonokok.
PEMERIKSAAN LABORATORIUM
C. Tes Definitif
Tes Oksidasi  Semua Neisseria  perubahan warna koloni dari merah
muda ke lembayung  Tes oksidasi  dilanjutkan dengan Tes fermentasi
dengan memakai glukosa, maltosa, sukrosa. N.g  hanya mengikat glukosa
saja
D. Tes Beta-Laktamase
Kuman mengandung enzim beta-laktamase  perubahan warna dari
kuning ke merah.
PEMERIKSAAN LABORATORIUM
E. Tes Thomson
Mengetahui sampai dimana infeksi berlangsung
Syarat:
 Setelah bangun pagi
 Urin dibagi 2 gelas
 TIDAK BOLEH MENAHAN KENCING dari gelas 1 ke gelas 2
 Syarat mutlak: kandung kencing harus mengandung air seni paling sedikit 80-100
ml. Jika kurang gelas 2 sukar dinilai karena baru menguras uretra anterior

F. ELISA  deteksi Antigen/Antibodi

G. DNA probes
 Gelas I Gelas II Arti

Jernih Jernih Infeksi (-)

Keruh Jernih Infeksi uretra anterior

Keruh Keruh Pan uretritis

Jernih Keruh Tidak mungkin

TREATMENT
URETHRITIS NON-SPESIFIK
DEFINISI
Infeksi uretra yg penyebabnya bukan o/k Neisseria gonorrhoeae

Penyebab:
 Chlamydia trachomatis (terbanyak)
 Ureaplasma urealyticum
 Trichomonas vaginalis
 Candida albicans
 HSV
 tdk diketahui (20%)
INFEKSI CHLAMYDIA
-Chlamydial Trachomatis Serotypes D-K menyebabkan STDs, genital infection.
- Bacteri sangat kecil
- Sub Type Chlamydial Trachomatis A,B,C  infection trachoma pada mata.
- Sub Type DK  genital infection
Pada laki-laki : Symptomatic
Pada wanita : Asymptomatic
- Sero Type L1,L2,L3  Lympho Granuloma Venerum (LGV) dan bisa systemic disease.
- Ocular infection pada bayi terjadi pada saat persalinan dan juga dapat menyebabkan
Chlamydial Trachomatis
- Pada bayi juga bisa menyebabkan Pneumonia Chlamydial Trachomatis.
DIAGNOSIS
Masa inkubasi:
Pria 1- 3 minggu atau lebih lama
Wanita sulit diketahui mungkin 1-4 minggu.
Gejala klinis : Px: - meatus eksternus eritem, edem; tdk ada radang
- discar uretra mukous, seromukous atau jernih,
Pria duh tubuh uretra, mukoid atau mukopurulen
mukopurulen,kadang-kadang purulen dapat
disertai eritema meatus
Wanita duh tubuh serviks muko-purulen, ektopia
serviks, serviks mudah berdarah.
PEMERIKSAAN LABORATORIUM
• Bakteri Chlamydia merupakan bakteri intraselular. Hal tersebut menyulitkan dalam
melakukan teknik kultur sebagai standar baku emas untuk diagnosa
•Pengambilan spesimen : menggunakan swab + medium tanpa antibiotik dikirim dgn
suhu -70 ºC. Demikian juga bila dalam 24 jam tak diperiksa.
•Kultur untuk C. trachomatis :
dgn medium telur yg mengandung embrio
• DFA (Direct Fluorescent Antibodi) dgn mikroskop UV :
Ambil jaringan yg terinfeksi ditambahkan fluorescein, conjugated monoclonal
antibodi selanjutnya dilihat dengan mikroskop dan terlihat Yellow green
URETHRITIS NON-SPESIFIK
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VAGINITIS Tamara Ayu Widyasuri & Zakia
IMO UROREPRO 2017
VAGINITIS
What is it?
Clinical syndrome caused by inflammation/infection of the vagina
Characterized by abnormal vaginal discharge
Sometimes caused by an STD
VAGINITIS ETIOLOGIES
 Bacterial Vaginosis (BV)
 Trichomoniasis
 Vulvovaginal Candidiasis (VVC)
PATHOGENESIS

Decreased Lactobacilli and Doderlein. – decreased lactic acid

causes increased pH

Overgrowth of anaerobes associated with increased enzymes

that breakdown vaginal peptides into amines that are
malodorous
PATHOGENESIS

Amines – involving to form fishy odour

At elevated pH – G. vaginalis adheres to squamous cells (“Clue cells”)

epithelium stratificatum squamosum non cornificatum. Dibatas o/ hart
line.
MICROBIOLOGY OF THE VAGINA
Vaginal epithelium sensitive to estrogen, which
induces production of glycogen
Lactobacillus spp. (normal flora) produce H2O2 and
metabolize glycogen to lactic and acetic acid to
keep pH at 3.8 - 4.2
Acidic pH and Lactobacillus spp. colonization inhibit
overgrowth of vaginal pathogens
If vaginal pH is increased, GNRs, anaerobes, yeast
and Gardnerella colonize vagina
NORMAL VAGINAL PHYSIOLOGY
Characteristic discharge
 1-4 ml fluid/24 hours
 White or transparent, thick, odorless
 Variation with cycle, OCPs, pregancy

pH 4-4.5
Microscopy shows squamous cells with rare PMNs
FACTORS ADVERSELY AFFECTING
NORMAL VAGINAL FLORA
Douching
Antibiotic and antifungal therapy
Hormonal changes: pregnancy, OCs
Spermicides, lubricant
Foreign bodies: tampons, IUD, diaphragm
Intercourse, semen
Menses
EFFECTS OF ESTROGEN STATUS ON VAGINAL
MICROFLORA
Microbial loads are 100x lower in prepubertal and post-menopausal women
compared to reproductive aged women
Estrogen and resulting glycogen deposition supports growth of both beneficial
bacteria (lactobacillus) and pathogens
VAGINITIS: CLINICAL PRESENTATION
Abnormal vaginal discharge
Vulvar itch
Odor
Discomfort
Burning with urination
Painful intercourse
VAGINITIS
CLINICAL EVALUATION OF
VAGINITIS
Physical Exam
Characteristics of vaginal discharge
Appearance of the vulva
Appearance of vaginal mucosa
Appearance of cervix
DIAGNOSTIC EVALUATION OF
VAGINITIS
Vaginal pH
Whiff test (amine test)
Microscopy
 Saline and KOH wet mounts
VAGINAL PH MEASUREMENT

Normal vaginal pH High vaginal pH (>4.5)

BACTERIAL VAGINOSIS A sexually-associated disease
BACTERIAL VAGINOSIS
Vaginal lactobacilli are replaced by large numbers of
Anaerobes:
Mobiluncus
Bacteroides spp.
Prevotella spp.  Haemophilus
 peptostreptococci
Aerobic GNRs: Gardnerella vaginalis
BACTERIAL VAGINOSIS
MICROBIAL SHIFTS IN BV
11
10

Bacteria
G vaginalis
Anaerobes
Mycoplasmas

Lactobacillus
4
10
100-1000 x increase in pathogenic bacteria
REVISED MODEL OF PATHOGENESIS

More partners/ Douching Absence of Lactobacilus

Frequent intercourse

Normal Bacterial Vaginosis

RF
Smoking
Non-white race

Hillier, The Secret Garden, Principles in STD/HIV Research, Seattle 2003

CLINICAL PRESENTATION
OF BV
Foul, “fishy” odor
Increased or changes in vaginal discharge
Vulvar itching and/or irritation
Symptoms worse after intercourse and during menses
50% may be asymptomatic
Risk factors: multiple sexual partners, douching, lack of lactobacilli
BV: DIAGNOSTIC CRITERIA
Amsel Criteria (3 of the following 4):
Homogeneous white noninflammatory discharge that adheres to the
vaginal walls
Vaginal pH > 4.5
Positive “whiff” test
> 20% Clue cells on saline wet mount

>90% sensitive
CLUE CELLS
 BV: TREATMENT
Recommended regimens:
 Metronidazole 500 mg PO BID x 7 d
 Metronidazole gel 0.75% 5 g per vagina QD x 5 d
 Clindamycin cream* 2% 5 g per vagina QHS x 7 d
Alternative regimens:
 Metronidazole 2 g PO x 1
 Clindamycin 300 mg PO BID x 7 d
 Clindamycin ovules 100 mg per vagina QHS x 3 d

*oil-based cream, may weaken condoms

and diaphragm
BV: RECURRENT INFECTION
Up to 85% will have recurrence within one year
25% within 4-6 weeks after treatment
Occurs equally often after vaginal or oral therapy, and after metronidazole
or clindamycin
No improvement in recurrence rates after treatment of male partners
TREATMENT
Vaginosis bacteria and trichomoniasis usually treated by Metronidazole 500mg twice
a day for7 day or 2gr single dose.
For pregnant woman use ampisilin or amoxicillin 5oomg q times a day for 5 day.
VULVOVAGINAL CANDIDIASIS (VVC)
VULVOVAGINAL CANDIDIASIS (VVC)
Caused by various Candida spp. (albicans 75-
90%, glabrata 5-10%, tropicalis 5-10%)
Candida may colonize 15-40% of women, so
only considered pathogen if symptoms present
In U.S., 13 million cases per year
Affects 70-75% of women during their lifetime,
with 40-50% having at least 1 recurrence
PELVIC EXAM
VVC: RISK FACTORS
Hormonal changes
Pregnancy
Diabetes
Antibiotic use
HIV infection
Steroids
VVC: CLINICAL MANIFESTATIONS
Abnormal discharge
Vaginal soreness ( rasa sakit)
Vulvar burning or itching
Dysuria may be only complaint
WHY DOES A WOMAN “GET” YEAST VAGINITIS?
Many women are colonized by yeast as part of normal flora
Yeast colonization more frequent among those having vaginal
lactobacilli, those who smoke, and women who are sexually active
Unknown why some women develop symptoms and others remain
asymptomatic
Exposure to irritants may increase sensitization by yeasts
DIAGNOSIS OF VVC
Accurate diagnosis is crucial to treatment success
--Signs and Symptoms
PLUS
--Positive saline and/or 10% KOH microscopy
OR
--Positive culture
Clinical signs and symptoms are not specific in VVC
VVC: DIAGNOSIS
Mucosa often inflamed and erythematous
Discharge is white, thick and curd-like( seperti air
susu/keju), or may be thin and watery
KOH wet mount with budding yeast or
pseudohyphae (50-70% sensitive)
pH usually normal
Fungal culture for non-albicans spp.
 Candidiasis Curriculum Diagnosis

PMNS AND YEAST PSEUDOHYPHAE

Saline: 40X objective Yeast

pseudohyphae

Yeast
buds
PMNs

Squamous epithelial cells

Source: Seattle STD/HIV Prevention Training Center at the University of Washington 63

 Uncomplicated VVC Complicated VVC

Occurrence Infrequent Frequent recurrence

Clinical
presentation Mild to medium Severe

Species of
fungus Candida albican Other Candida sp.

Host status Immunocompetent Immunoincompetent

Response to Good Poor

therapy
UNCOMPLICATED
Topical Therapies:
VVC: TREATMENT
Kotrimazol 500mg PV SD + ketokonazol 200mg
SD atau itrakonazol 2x200mg SD
Oral Therapy:
Fluconazole 150 mg PO x 1

*Topical therapies are oil-based and may weaken condoms and

diaphragm These medications are available by prescription
TRICHOMONAS VAGINALIS A sexually transmitted infection
TRICHOMONAS: A PATHOGEN OVER LIFETIME
Etiologic agent: Trichomonas vaginalis, flagellated anaerobic
protozoa
Can be transmitted to prepubertal girls through sexual abuse
Little evidence to support transmission through shared towels, toilet
seats, etc.
Can be carried asymptomatically for years
TRICHOMONIASIS
CLINICAL PRESENTATION
May infect ectocervix, vagina, urethra or bladder
In women, causes malodorous yellow-grey discharge with irritation and vulvar itching
In men, can cause urethritis
Often asymptomatic ( 50%)
TRICHOMONIASIS: DIAGNOSIS IN
WOMEN
Typical vaginal discharge: thin, frothy,
grey/yellow
May see punctate cervical hemorrhages
(strawberry cervix) 5 -10%
Motile trichomonads on saline wet mount
(sensitivity may be as low as 60%)
pH > 4.5
Whiff test may be positive
Culture available (InPouch TV Test)
PCR tests exist but not FDA approved
TRICHOMONAS VAGINITIS
PELVIC EXAM
TRICHOMONAS VAGINALIS
TRICHOMONAS VAGINALIS

Seattle STD/HIV Prevention Training Center

TRICHOMONIASIS: TREATMENT
Recommended regimen:
 Metronidazole 2 g PO x 1*
 Tinidazole 2g PO x 1

Alternative regimen:
 Metronidazole 500 mg PO BID x 7d

Metronidazole highly effective: 95% if both partners

treated
*Recommended regimen is the same in pregnancy
ULKUS MOLE / CHANCROID
Definisi : ulkus genital akut, local dan dapat berinokulasi sendiri dan disertai supurasi
KGB regional
Etiologi : Haemophillus ducreyi. ( Gram – dan tidak berkapsul)
Inkubasi 3-7 hari tanpa gejala prodromal, memanjang pd HIV.
UKK awal papul inflamasi yg akan berkembang menjadi ulkus dlm 1
-2 hari. Ulkus multiple,dangkal, tdk indurasi,sangat nyeri, tepi
Bergaung,rapuh,tidak rata dan eritem di sekeliling ulkus. Dasar ulkus
Dilapisi eksudat nekrotik kuning dan dapat menyebar sendiri.
Laki2: frenulum,preputium,sulcus coronaries
Pr : introitus,vestibulum,labia mayor
Varian ulkus:
- dwarf chancroid : lesi kecil,dangkal,dd
herpes genital, tdk nyeri
- giant chancroid : soliter, besar, ada di
lokasi bubo inguinal
-follicular chancroid: pd pr di labia
mayor&pubis
-transient chancroid: ulkus sangat dangkal
dan segera sembuh diikuti bubo
-phagedenic chancroid(molle
gangrenosum):ulkus nekrotik akibat infeksi
sekunder fusospirocheta
- serpiginous chancroid : ulkus bergabung
dan meluas
-popular chancroid(molle elevatum) : papul
berulserasi granulomatosa, dapat
menyerupao donovanosis/kondilomalatum
-mixed chancroid: ulkus mole yg nyeri tanpa
indurasi yg dapat bersama dengan ulkus
sifilis
KOMPLIKASI:
Adenitis inguinal, fimosis/parafimosis, fisura
uretra, fistel rektovagina dan infeksi
campuran
PX : ISOLASI BAKTERI, PCR, KULTUR
DX : TEMUAN KULTUR
DD: SIFILIS PRIMER, LGV
TALAK :
Ciprofloxacin 500mg 2x1 PO selama 3
hari ATAU
Eritromisin 500mg 4x1PO selama 7 hari
ATAU
Azitromisin 1gr PO SD ATAU
Ceftriaxone 250mg IM
Jika bubo >5cm di aspirasi.
Luka di kompres saline
SYPHILIS (LUES) Pidha
Universitas Lambung Mangkurat
DEFINITION
Syphilis is a systemic disease caused by Treponema pallidum that is sexual transmiitted
sexually or by other intimate contact; could also from pregnant woman to her fetus
in utero or contact directly with maternal lesion.

Sifilis adalah penyakit yang disebabkan oleh infeksi bakteri Treponema pallidum
yang bersifat akut dan kronis ditandai dengan lesi primer diikuti dengan erupsi
sekunder pada kulit dan selaput lendir, kemudian masuk ke dalam periode laten
diikuti dengan lesi pada kulit, lesi pada tulang, saluran pencernaan, sistem saraf
pusat dan sistem kardiovaskuler.
PATHOGENIC TREPONEMAS
* Bentuk spiral helix (spirochete)
* Panjang: 6-15 m; lebar: 0,1-0,2 m, Diameter 5-15 m
Punya membran luar (OM) yg dikelilingi
- flagela periplasmik,
- Kompleks membran peptidoglikan-sitoplasmik
- Silinder protoplasmik
OM sangat berbeda dengan bakteri gram (-) lain yang dimana :
1. LPS tidak ada , 2. Porin tidak ada, 3. Sangat sedikit protein dalam membrannya
* Multiplikasi dg pembelahan biner
* Tdk dpt dikultur in-vitro dan gram stain
* sangat sedikit antigen di permukaannya, sehingga membuatnya memiliki peralatan yg tersembunyi
oleh sistem imun kita
 ABOUT TREPONEMA
•Bakteri motil, gram negatif

•Gerakannya berupa rotasi sepanjang aksis dan

maju gerakan pembuka botol

•Penularan sifilis dapat melalui hubungan seksual,

dapat terjadi secara vertikal dari ibu kepada janin
dalam kandungan atau saat kelahiran, melalui
poduk darah atau transfer jaringan yang telah
tercemar, dan kadang-kadang dapat ditularkan
melalui alat kesehatan
 Syphilis Yaws Bejel Pinta

Organism T.P subs pallidum T.P subs pertenue T.P subs endemicum T. carateum

Transmission Sexual contact Skin contact Skin contact oral Skin contact

Lesion type
Primary Chancre (durum) Crusted papules Oral mucosal lesion Crusted papules and
paques

Secondary Macular or Papillomatous and Mucous patches and Scaly plaques

papulosuamous scarring condyloma lata

Tertiary Gummata and Gummata of bone and Gummata of catilage, Dyschromia

endarteritis skin bone, and skin
KLASIFIKASI
1. Sifilis Akuisita
 S.dini S.Primer
S. Sekunder
S. Laten dini
 Lanjut  S. Laten lanjut
S. Tersier
S. Kardiovaskuler
Neurosifilis
2. Sifilis Kongenital
SIFILIS STAD. PRIMER
3 mgg setelah CS
papula- erosi, keras, permukaan tertutup krusta
ulkus di daerah genital eksternadurum (tidak nyeri)
tunggal/multipel, uk 1-2 cm
- tepi meninggi, keras
- pembesaran lln. Inguinal bilateral
- sembuh spontan 4-6 mgg (30 hr)
SIFILIS STAD. SEKUNDER
Lesi-lesi skunder yg menyerupai
penyakit kulit lain, seperti ruam
makulopapuler merah di seluruh kulit,
dan papula pucat basah (kondiloma)
pada daerah anogenital, ketiak, dan
mulut.
S II umumnya tidak gatal disertai
limfadenitis generalisata. Lesi
skunder juga sembuh secara spontan.
lesi kulit simetris, makula, papula, folikulitis, papuloskuamosa,pustula
papula basah daerah lembab: kondilomata lata
lesi pd mukosa mulut, kerongkongan, serviks: plakat
alopesia : moth-eaten alopecia --> oksipital
SIFILIS STAD. LATEN AWAL
-Disebut juga Sifilis Laten Asimtomatik
-6 bulan setelah stadium sekunder
-Ditandai dengan serologi positif namun tidak ada
manifestasi klinis dari sifilis
 EARLY SYPHILIS
Persisten selama 4-10 mgg setelah Stadium latent
Primary Infection Syphillis

Syphilis

Syphilis
Secondary Infection

Early Latent Infection

4-6 minggu fase primer & asimptomatis
setelah kontak persisten sampai 6 bulan setelah
Ulkus durum 24 bulan stadium sekunder
(soliter, dasar Lesi Serologi (+)
bersih, indurari, mucocutaneous, asimptomatis
tidak nyeri) berhubungan
dengan end
artery
Moth eaten
alopecia
 EARLY SYPHILIS
Primary Infection Syphilis Secondary Infection Syphilis EARLY LATENT INFECTION SYPHILIS

ASIMPTOMATIK !
BUT SEROLOGY (+)
 PATHOGENESIS OF SYPHILIS
stage of disease signs and symptoms
initial contact
2-10 weeks (depends on primary chancre at site of
Inoculum size) infection
primary syphilis enlarged inguinal nodes
spontaneous healing
1-3 months
secondary syphilis flu-like illness
4-6 weeks myalgia, headache, fever
mucocutaneous rash
spontaneous resolution
latent syphilis
3-30years
tertiary syphilis neurosyphilis;
general paralysis of the
insane, tabes dorsalis
cardiovascular syphilis;
aortic lesions, heart failure
progressive destructive
disease
pathogenesis
multiplication of treponemes at
site of infection; associated host
response
proliferation of treponemes in
regional lymph nodes
multiplication and production of
lesions in lymph nodes, liver
joints, muscles, skin and mucous
membranes
treponemes dormant in liver and
spleen
re-awakening and
multiplication of treponemes
further dissemination and invasion
and host response (cell-mediated
hypersensitivity)
gummas in skin, bone, testis
 6 weeks Approx Approx
To 6 month 18 month 18 month

Infection

Primary Secondary Latent Syphilis

Tertiary
(Chancre) (Rash) (No sign of disease)

Incubation Benign gummatous

Period 9-90 Cardio-vascular
days syphilis
Neurosyphilis

1-2 years Many years

To a lifetime

Early Syphilis Late Syphilis

PATHOGENESIS
Masa inkubasi ± 2-10 minggu rata-rata 3 minggu
Primary lesion dihubungkan dengan lymphadenophaty
Secundary (Bacterimic) stage dihubungkan dengan general mucocutaneus
lesion.
Tertiary stage charakteristik dengan progressive destructive, mucocutaneus
musculoskletal atau parenchymeal lesion, aortitis, atau symptomatic
central nervous system disease.
LATE SYPHILIS
The late manifestations of syphilis fall into three main types : cardiovascular, benign
gummatous, and neurosyphilis. The common underlying pathophysiology event
appears to be an endarteritis and periarteritis of small and medium sized vessels.

 Hyperplastic endothelial cells

 Lymphocytes infiltrating media and
adventitia
 Eccentric internal Hyperplasia
LATE SYPHILIS
A. Cardiovascular Syphilis
This form of late syphilis is uncommon today, it has been estimated to occur in
approximately 10% of cases of untreated syphilis
The major pathologic changes in cardiovascular syphilis are dilatation of aortic ring with
incompetence of valve, LVH, Aortic dilatation with aneurysm formation, stenosis coronary
artery.
B. Benign Gummatous Syphilis
This is probably represent a severe inflamatory response to treponemal antigens. Skin
and bones are affected most commonly. Skin lesion maybe nodular( multiple, groups,
asymetric), noduloulcerative or gummatous. They are chronic, painless, and slowly
progressive and are found most often on the face, trunk, and extremities.
LATE SYPHILIS
C. Neurosyphilis
T.Palidum invades meninges and neural tissue during secondary stage of disease.
Spirochetes maybe seen in CSF, and in ocular and middle ear fluid.
A chronic, low grade meningitis with lymphocytic infiltration of the meninges. An
endarteritis of small vessels of the brain and spinal cord
diagnostic criteria of Asymptomatic neurosyphilis are :
1. Reactive CSF VDRL
2. Ractive Serum treponemal test
3. Five or more lymphocytes/ mm3 CSF
4. CSF total protein ≥ 45 mg/dL
DIAGNOSIS
1. Spesimen :
• Eksudat lesi
• Darah
2. Darkfield Examination
3. Immunofluorescence
4. Serologic Test for Syphilis (STS)
COLLECTION OF SPECIMENS
Specimens for dark field microscopy can be collected from primary chancre, moist
secondary lesion or from lymph nodes
Specimens for the direct immunofluorescent antibody test for T.Palidum can be
collected from oral and anal lesion. The idel specimen is serous fluid with minimal
RBC.
 DARKFIELD EXAMINATION
Pengecatan :
a. Impregnasi perak
b. Negatif
Paling baik : dengan mikroskop lapangan gelap
 kuman yang hidup
Terdiri dari 3 gerakan :
 Undulasi
 Cork-screw (pembuka botol)
 Maju mundur
 DIRECT FLUORESCENT ANTIBODY TEST
DFAT-TP is used to diagnose late stage
adult or congenital syphilis, or to
distinguish skin lesion or secondary or
late syphilis from those lyme disease, or
primary lesion herpes and chancroid
SEROLOGIC TEST FOR SYPHILIS
Infeksi treponemal pallidum menghasilkan 2 tipe antibodi :
1.Spesifik antibodi  polipeptida dari bakteri.
2.Nonspesifik antibodi (reagin antibodi)  non-treponemal antigen disebut
cardiolipin.
SEROLOGIC TEST FOR SYPHILIS (STS)
Non treponemal and Treponemal
A. Non Treponemal Serologic Test
Detect IgM and IgG antibodies to lipoidal material released from damaged host
cells, as well as to cardiolipin like material released from treponeme. All non
treponemal test will occasionally give false-positive (Titer less than 8). Diulang 1
minggu, 1 bulan dan 3 bulan (jika non reactive “BUKAN SYPHILIS”)
1. Venereal Disease Research Laboratory (VDRL) – Microscopic Test
2. Unheated Serum Reagen (USR) – Microscopic Test
3. Rapid Plasma Reagen (RPR) – Macroscopic Test
4. Toluidine Red Unheated Serum Test(TRUST) – Macroscopic Test
SEROLOGIC TEST FOR SYPHILIS (STS)
B. Treponemal Serologic Test
Test konfirmatif setelah tanda2 klinis yang nampak/ RPD dan hasil yang reaktif
pada serologi non-treponemal. They are qualitative procedure, which therefore they
cannot be used to monitor efficiacy of treatment.
1. Fluorescent Treponemal Antibody Absorption (FTA-ABS) & FTA-ABS DS(Double
Strain)
Initial Test Repeat Test Interpretation of Fluorescent report
2+ to 4+ .... Reactive
1+ >1+ Reactive
1+ =1+ Reactive minimal*
<1+ Non-Reactive
SEROLOGIC TEST FOR SYPHILIS (STS)
2. T.Palidum Hemagglutination Assay (TPHA) & TP-PA (Passive Particle Agglutination
Assay)
A reactive test at a titer of 1:80 is considered positive.
3. Treponemal Enzyme Immunoassays (EIA)
4. Treponamal Rapid Test
TREATMENT
A. Primary and Secondary Syphilis
Benzathine Penicilin G 2,4 juta unit I.M SD (Dewasa)
Benzathine Penicilin G 50.000 Unit/KgBB I.M
Clinical and serologic evaluation should be performed at 6 and 12 months after treatment; more
frequent evaluation might be prudent if follow-up is uncertain or if repeat infection is a concern.
B. Late Syphilis
Benzathine penicillin G 2.4 million units IM in a single dose (Early in adults)
Benzathine penicillin G 7.2 million units total (Late in adults) bagi 3 dosis interval 1 minggu
Benzathine penicillin G 50,000 units/kg IM, up to the adult dose of 2.4 m units in SD (child)
Benzathine penicillin G 50,000 units/kg IM, up to the adult dose of 2.4 m units in SD (child) x3
TREATMENT
Tertiary Syphilis
Benzathine penicillin G 7.2 million units total, administered as 3 doses of 2.4 million
units IM each at 1-week intervals
Neurosyphilis & Occular Syphilis
Aqueous crystalline penicillin G 18–24 million units per hari, masukkan 3–4 juta unit
I.V setiap 4 jam atau infus selama 10–14 days.
Alternative : (BOTH)
Procaine penicillin G 2.4 million units IM once daily
Probenecid 500 mg orally four times a day, both for 10–14 days
SPECIAL CONSIDERATION
A. Penicilin Allergy
Doxycycline 100mg 2x (14 hari) + tetracycline 500mg 4x (14 hari)
Although limited clinical studies, along with biologic and pharmacologic evidence,
suggest that ceftriaxone (1–2 g daily either IM or IV for 10–14 days)
Azithromycin as a single 2 g
B. Pregnancy
Pregnant women should be treated with the penicillin regimen appropriate for their
stage of infection.
CONGENITAL SYPHILIS
Screening terbaik saat kunjungan prenatal pertama kali ! Uji serologic tambahan
saat usia gestasi 28 wks dan saat kelahiran.
The diagnosis of congenital syphilis can be difficult, as maternal nontreponemal
and treponemal IgG antibodies can be transferred through the placenta to the
fetus, complicating the interpretation of reactive serologic tests for syphilis in
neonates.
All neonates born to mothers who have reactive nontreponemal and treponemal test
results should be evaluated with a quantitative nontreponemal serologic test (RPR or
VDRL) performed on the neonate’s serum.
SIGN OF CONGENITAL SYPHILIS
1.Keratitis interstitialis
2.Gigi Hutchinson
3.Gigi Mullberry
4.Gangguan syaraf pusat VIII (ketulian)
5.Neurosifilis
6.Kelainan pada tulang
7.Kelainan pada kulit
8.Lesi kardiovaskuler (aortitis)
9.Gambaran muka menunjukkan saddlenose
SCENARIO 1: PROVEN OR HIGHLY PROBABLE
CONGENITAL SYPHILIS
Any neonate with:
1. an abnormal physical examination that is consistent with congenital syphilis; OR
2. a serum quantitative nontreponemal serologic titer that is fourfold higher than the
mother’s titer; OR*
3. a positive darkfield test or PCR of lesions or body fluids.
SCENARIO 2: POSSIBLE CONGENITAL SYPHILIS
Any neonate who has a normal physical examination and a serum quantitative
nontreponemal serologic titer equal to or less than fourfold the maternal titer and
one of the following:
1. mother was not treated, inadequately treated, or has no documentation of having
received treatment; OR
2. mother was treated with erythromycin or a regimen other than those recommended
in these guidelines (i.e., a nonpenicillin G regimen); †† OR
3. mother received recommended treatment <4 weeks before delivery.
SCENARIO 3: CONGENITAL SYPHILIS LESS LIKELY
Any neonate who has a normal physical examination and a serum quantitative
nontreponemal serologic titer equal to or less than fourfold the maternal titer and
both of the following are true:
1. mother was treated during pregnancy, treatment was appropriate for the stage of
infection, and treatment was administered >4 weeks before delivery and
2. mother has no evidence of reinfection or relapse.
SCENARIO 4: CONGENITAL SYPHILIS UNLIKELY
Any neonate who has a normal physical examination and a serum quantitative
nontreponemal serologic titer equal to or less than fourfold the maternal titer and
both of the following are true:
1. mother’s treatment was adequate before pregnancy and
2. mother’s nontreponemal serologic titer remained low and stable (i.e., serofast)
before and during pregnancy and at delivery (VDRL <1:2; RPR <1:4).
RECOMMENDED EVALUATION
Only needed for Proven-Possible syphilis !

• CSF analysis for VDRL, cell count, and protein**

• Complete blood count (CBC) and differential and platelet count
• Other tests as clinically indicated (e.g., long-bone radiographs, chest radiograph,
liver-function tests, neuroimaging, ophthalmologic examination, and auditory brain
stem response).
TREATMENT
Aqueous crystalline penicillin G 100,000–150,000 units/kg/day, administered as
50,000 units/kg/dose IV every 12 hours during the first 7 days of life and every 8
hours thereafter for a total of 10 days OR
Procaine penicillin G 50,000 units/kg/dose IM in a single daily dose for 10 days
OR
Benzathine penicillin G 50,000 units/kg/dose IM in a single dose
THANK YOU
HERPES SIMPLEKS