Bakteri,Virus dan Jamur

Penyebab Infeksi pada

Kulit dan Jaringan Lunak

Pror. Dr. dr. Efrida Warganegara, M.Kes., Sp.MK

Infeksi Kulit oleh M.O

Kulit merupakan barrier pertahanan yang baik

terhadap infeksi bakteri.

Walaupun banyak bakteri hidup di kulit, mereka tidak
menimbulkan suatu infeksi
Infeksi bakteri pada kulit dapat mempengaruhi suatu
noda/bintik tunggal, terlihat sbg pimple atau dapat
menyebar dalam 1 jam-an, mempengaruhi suatu are
yg luas
Infeksi kulit dapat luas sifat seriusnya penyakit,
mulai dari paling ringan (Acne) sampai kondisi
mengancam kehidupan (Staphylococcal Scalded
Skin Syndrome)

Infeksi Kulit oleh M.O

Banyak tipe bakteri yg dapat menginfeksi kulit, yg

paling sering Staphylococcus dan Streptococcus

Pada beberapa orang mempunyai resiko tinggi utk
mendapat beberapa infeksi, mis:
- pend. Diabetes memp. aliran darah yg
sedikit ke kulit, khususnya tangan dan kaki
- pend. dgn AIDS krn sistem imun yg tertekan
Kelainan kulit oleh sinar matahari, garukan, atau
iritasi lain juga memungkinkan utk mendapat
infeksi.
Kenyataannya suatu pecahnya / kerusakan kulit
merupakan prodisposisi bagi seseorang utk
infeksi

Infeksi Kulit oleh M.O

Yg penting menjaga kulit tidak rusak dan

membersihan kulit mencegah infeksi. Jika kulit

terpotong atau tergaruk, mencuci area tsb dgn
sabun dan air membantu mencegah infeksi
Walaupun kebanyakan cream atau zalf antibiotik
sedikit mencegah / mengobati infeksi kulit, bbp
cream (Muciprocin) efektif utk bbp infeksi kulit
Merendam hangat dapat meningkatkan suplai
darah pada area infeksi dan membantu
membersihkan infeksi utk area yg kecil
Sekali infeksi menyebar, antibiotik harus diberikan
internal (mulut atau injeksi)

Infeksi Kulit oleh M.O

Infeksi spesifik pada kulit :
A. Oleh Bakteri
1. Staphylococcus, Streptococcus
2. B. anthrax, C. gas gangrene, M. leprae
3. Y. pestis, F. tularensis
B. Oleh Virus
1. Herpes (Simpleks, Zozter)
2. Smallpox, Varicella
3. Warts, Molluscum contagiosum
4. Morbilli, Rubella,
C. Oleh Jamur
1. Dermatophytosis, Phytiriasis versicolor,
2. Candidiasis

PYOGENIC COCCUS

Oleh :
Prof.Dr.dr. Efrida Warganegara, M.Kes., Sp.MK

PYOGENIC COCCUS
Pyogenic coccus :
adalah kokus yang menyebabkan
penyakit infeksi dengan produksi Pus.
Piogenik kokus dibagi kedalam :
1. Gram Positif : - Staphylococcus
- Streptococcus
2. Gram Negatif : - Neisseria

STAPHYLOCOCCUS

Oleh :
Dr. dr. Efrida Warganegara, M.Kes., Sp.MK

1. STAPHYLOCOCCUS AUREUS
Taxonomy
Family : Micrococcaceae
Genus
: Staphylococcus
Spesies : lebih dari 133 spesies,
spesies
yang penting sebagai
penyebab penyakit.
- Staphylococcus aures -> spesies
paling
penting

- Staphylococcus epidermidis
- Staphylococcus saprophyticus

1. STAPHYLOCOCCUS AUREUS

Kharakteristik Umum
- Gram (+) kokus, tersusun dlm gerombolan
- Catalase positif (+)
- adalah satu-satunya Coagulase (+) dan
hemolytic
- mungkin merupakan flora normal dari
carrier,
biasanya terdapat di hidung, atau perineum
- adalah penyebab infeksi pada host dengan
kateterisasi, pembedahan dll.

1. STAPHYLOCOCCUS AUREUS

Insidensi resistensi terhadap

antibiotik tinggi, misal -laktam
atau kebanyakan antibiotik lain.
- Infeksi >>> :adanya benda asing
dalam tubuh
-

1. STAPHYLOCOCCUS AUREUS

Faktor Patogenesitas
1. Coagulase
2. Toksin-toksin Cytolytic ( , , , , dan
leukocidin)
3. Enterotoksin yang disekresikan oleh beberapa
strain
4. TSST-1 (Toxic Shock Syndrome Toxin-1), dulu
dinamakan enterotoxin F
5. Exfoliatin yang dproduksi oleh Faga group II
6. Protein A adalah antiphagocytic (mengikat Fc
dari
Ab)
7. Teichoic acid melekat pada peptidoglycan

1. STAPHYLOCOCCUS AUREUS

Penyakit Klinik
Infeksi Kulit : impetigo, foliculitis,
furuncle, luka operasi, infeksi luka
bakar atau infeksi lesi traumatik.
Scalded skin syndrome exfoliatins
toxins
Infeksi S. aureus lain : Toxic Shock
Syndrome (TSS), Keracunan Makanan,
pneumonia, osteomyelitis & endocarditis.

1. STAPHYLOCOCCUS AUREUS

Diagnosis Laboratorium
- Kokus Gram positif, terdapat
dalam jaringan yang
infeksi
dalam bentuk berpasangan, atau
rantai pendek (pada media padat
tumbuh khas bergerombol)
- Tumbuh dengan -hemolysis

1. STAPHYLOCOCCUS AUREUS
Pengobatan
a. Drainase lesi
sama pemberian

: penting dilakukan
antibiotika

b. Test kepekaan terhadap antibiotik

dilakukan

bersamaharus

c. Bagi m.o. yang bukan penghasil penisilinase

diberikan penisilin G
d. Bagi m.o. penghasil penisilinase
Resisten Penisilinase

beri Penisilin

1. STAPHYLOCOCCUS AUREUS

Pengobatan (lanjutan)
e. Staphylococcus aureus resisten

metisilin (MRSA) :
menyebabkan resisten pd semua
obat -laktam & kebanyakan
antibiotika lainnya kondisi ini
dith/.dgn vancomisin atau
vancomisin+antibiotika lain.

1. STAPHYLOCOCCUS AUREUS

Prevention

- Memutus transmisi (cuci tangan,

desinfektans yang efektif), atau
pengurangan Staphylococcus dari
pakaian (> 700 C atau dry cleaning)
- mengurangi karier
- Berani menggunakan antibiotika
preoperatif dosis tinggi

STREPTOCOCCUS

Streptococcus
Taxonomy
Family : Streptococcaceae
Genus : Streptococcus, ada 3 tipe
pada LAD

Spesies yang penting :

1. S. pyogenes (group A, -hemolitik
Streptococcus)
2. S. pneumoniae ( - hemolytik)
3. S. viridans (-hemolitik)

hemolitik

1. Streptococcus pyogenes
Kharakteristik Umum
* Gram (+) kokus, tersusun tunggal,
berpasangan, atau seperti
rantai tergantung lingkungan
* Bersifat Fakultatif anaerob
* Melekat pada permukaan sel
melalui bagian asam
lipoteichoat dari pili

epithel

1. Streptococcus pyogenes
B. Klasifikasi
- Diklasifikasi sebagai group A dari 21 group
Lancefield
Streptococcus,
- mengandung spesifik KH dan beberapa protein Ag
T, R Ag) dlm dinding sel
- Diklasifikasi kedalam -hemolitik (dari , , dan
hemolitik)
- Sensitif terhadap Bacitracin
- Bersifat catalase negatif
- Jarang menjadi resisten terhadap penisilin
- Dapat dideteksi dari usap tenggorokan

(M,

1. Streptococcus pyogenes
Faktor Pathogenisitas
- Mempunyai Protein M -> suatu faktor virulensi
yang potensial fimbriae
- Mempunyai suatu kapsul asam hialuronat,
antifagositik, nonantigenik
- Toksin Eritherogenik diproduksi oleh
lisogenik
- Mempunyai 2 hemolisin : S dan O

strain

1. Streptococcus pyogenes
Penyakit Klinik
1. Faringitis Streptokokus
2. Scarlet fever

3. Infeksi Kulit : Impetigo,

Sellulitis, Erisipelas,
Fascitis
4. Post Infection Disease :
- rheumatic Fever
- Glomerulo Nephritis Acuta (GNA)

Bacillus anthracis

TAXONOMY
Family : Bacillaceae
Genus : Bacillus
Spesies yang penting:
Bacillus

anthracis (penyebab penyakit

anthrax)

Bacillus

cereus (penyebab keracunan

makanan)

Genus Bacillus
-

Basil gram (+), batang besar & variasi (bentuk cocobacillus sp

btk filamen), tsusun spt rantai panjang

Bersifat aerob, pembentuk spora,

kebanyakan saprofit di tanah, air, udara, &tumbuhan.

Kadang-kadang dpt menyebabkan infeksi pd org yg

imunocompromized (meningitis, endocarditis, GE)

Morfologi & Identifikasi :

-

Ukuran 1 x 3-4 um, memp. ujung sel yg segiempat, tersusun spt

rantai panjang, spora terletak ditengah, nonmotil.

Morfologi koloni : terlihat cut glass bila kena cahaya,

hemolisis tdk umum utk B.anthracis

Bacillus anthracis
KARAKTERISTIK UMUM
Ukuran : P : 3 5 um, L : 1 - 1,5 um
Koloni : - Pd agar darah : putih abu-abu, bulat,

permukaan tdk rata, bentuk

medusa
head, ground glass
appereance, non
motile, non
hemolisis.

- Pd agar tegak : mirip pohon cemara terbalik

Spora :
- endospora terletak ditengah & berbentuk
elips diantara basil yang bergerak,
- resisten thdp (perubahan lingkungan,
pemanasan, disenfektan kimia),
- hidup lama dlm tanah kering.

Zoonosis : dari hewan ternak ke manusia.

Hewan : sapi, kambing, domba, babi, kuda
dsb.
Sumber penularan : feses, urine, saliva yg
mengandung spora Bacillus anthracis
Produk hewan yang terkontaminasi spora
antrax baik itu kulit, bulu, rambut, wool
maupun tulang hanya dpt disterilkan dngn
autoclave.

B. PATOGENESIS

Patogen utama genus bacillus

Manusia terinfeksi dari hewan ternak

Cara penularan:

Luka pd kulit dan selaput lendir

Anthrax cutaneus

Melalui gigitan vektor (nyamuk dan

lalat)
Anthrax cutaneus

Inhalasi pernafasan Pulmonary

anthrax

Konsumsi daging yg terkontaminasi

Anthrax gastrointestinal

Faktor virulensi
1. Exotoksin :
- kompleks protein karbohidrat
atau protein saja
- dipengaruhi plasmid, kalau
plasmid hilang toxin tidak
diproduksi
- terdiri dari:
- PA (antigen protektif),
- EF (faktor edema),
- LF (faktor letal).
Respon toxic yg sering ditemui : edema
kulit dan menimbulkan kematian.

2. Simpai/Kapsul :
- mukoid,
- polipeptida (D-asam
glutamat),
- BM tinggi,
- antipagositik,
- tdk imunologik.

C. GEJALA KLINIS

Pada manusia kuman anthrax dapat

menyebabkan:
Anthrax cutaneus

95% kasus anthrax di AS, inkubasi : 2 5 hr

Disebut jg malignant pustule
Pd peternak dan pekerja di rumah
pemotongan hewan

Mekanisme :
- Spora masuk

12 36 jam germinasi di jaringan

pertumbuhan vegetatif
menyebabkan edema gelatinosa & kongesti papula
erhytema
vesikel
pustula
ulkus nekrotik
menyebar ke KGB
ke sirkulasi darah
septikemik fatal

Erhytema papule setelah 7-10 hr akan membetuk luka

menghitam yang dikelilingi edema disebut juga
Central Black Eschar
Ditandai : edema, lymphangitis, lympadenopathy,
demam, malaise, sakit kepala, meningitis

D. LABORATORIUM

BP : cairan,pus dr lesi, darah, sputum

Pewarnaan gram, tampak basil gram +, batang
besar, rantai panjang
Pewarnaan fluorosensi umum digunakan pd sediaan
kering
Biakan :
- Agar darah : koloni putih abu-abu, nonhemolitik, tekstur kasar (ground glass
appereance)
- Semi Solid : non motile
BP disuntikkan intraperitoneal pd mencit /
marmut, yg berisi pus dari kuman menyebabkn
mencit / marmut akan mati

Imunisasi anthrax berdasarkan percobaan

Louis Pasteur (1881). vaksinasinya
menggunakan basil hidup yg dilemahkan,
suspensi spora, antigen protektif dari
filtrat biakan.

E. PENGOBATAN

Antibiotik : Penisilin (DOC), Streptomisin,

Tetrasiklin, Eritromisin, Klindamisin.

Efektif sebelum terjadi bakteriemia, kurang

efektif bila toxinnya telah terbentuk.

F. PENCEGAHAN
- Kremasi dan mengubur bangkai hewan
- Vaksinasi hewan ternak
- Imunisasi orang yg beresiko terinfeksi
krn tempat dan pekerjaannya
- Dekontaminasi menggunakan autoclave
barang (sarung tangan / baju) yg
digunakan saat menangani hewan yg
terinfeksi, juga pd produk-produk hewan.
- Membatasi pergerakan hewan ternak.

Mycobacterium leprae
Organism ditemukan oleh Hansen pada

tahun 1873 (9 th sebelum Kochs

menemukan basil tubercle)

Tidak dapat dibiak pada media bakteriologi

artifisial (nonliving)
Khas bakteri tahan asam, tunggal, paralel
dalam ikatan atau dalam massa yg secara
reguler didapati dari kulit atau membrana
mukosa (khususnya septum nasal) pada
leprosy lepromatous

 Basil

sering dijumpai dalam sel endotel

pembuluh darah atau sel mononuklear

Organismse

tak dapat tumbuh pada

media artifisial

Jika

basil dari leprosy manusia(kerokan

bag.dalam jar.nasal) diinokulasi pada
tapak kaki mice, lesi granulomatous
lokal berkembang dengan multiplikasi
basil yg terbatas

Inokulasi

pd armadillos berkembang
leprosy lepromatous yang ekstensif

Gejala Klinik
- Onset leprosy insidious
- Lesi melibatkan jaringan tubuh yang dingin
: skin, syaraf superficial, hidung,
pharynx,
larynx, mata & testicles
- Gangguan Neurologi dimanifestasi melalui
infiltrasi syaraf & penebalan,
menghasilkan anesthesia, neuritis,
paresthesia, ulkus tropic & resorbsi
tulang & pemendekan dari jari

2 tipe utama penyakit

Lepromatous
- penyakit progresif, malignan, lesi
kulit nodular, melibatkan syaraf
simetri yang lambat,
bertumpuknya basil tahan asam
pd lesi kulit, bacteriemia terus
menerus, test kulit lepromin
negatif
- CMI : berkurang, kulit diinfiltrasi
oleh T sel suppressor

Tuberculoid
- Perjalanan penyakit jinak dan
nonprogresif, lesi kulit macular,
melibatkan syaraf asimetris yg
berat
secara mendadak, beberapa basil ada
pada lesi, test kulit lepromen positif,
- CMI intak & infiltrasi kulit dgn T
cells helper
Several

intermediate stages

Diagnosis Laboratorium :
Kerokan dengan scalpel dari
kulit
atau dari mukosa nasal atau dari
biopsi dari kulit cuping telinga
(earlobe)
Smear pada slide, dicat
dengan
ZN
Tak ada test serologi yang bernilai

Treatment :

Beberapa sulfon yg spesifik (misal

dapson,
DDS) & rifampin menekan
pertumbuhan dari

M. leprae & manifestasi klinik dari leprosy

jika
diberikan untuk waktu berbulan-bulan

Clofazimine adalah obat peroral yang

diberikan untuk leprosy yang resisten sulfon

Epidemiology :
Transmission paling mungkin terjdi
jika anak kecil terekspose dalam
waktu lama dengan basil yg
banyak
Sekresi Nasal adalah material
infecsius yang opaling mungkin bagi
kontak dalam keluarga
Masa Inkubasi mungkin sekitar 2
10
tahun

Coccobacil Francisella tularensis

Patogenesis :
- F. tularensis sangat infectious, masuk melalui aberasi
kulit, membrana mukosa dan inhalasi dgn sejumlah 50
bakteri dapat menyebabkan infeksi
- Inkubasi 2-6 hari, inflamsi, tumbuh papula yang
berulkus, kel. Limpe regional besar & necrotik,
kadang-kadang mengering dlm bbp minggu
- Infeksi melalui inhalasi aerosol menyebabkan radang
peribronkhial, pneumonia yg terlokalisir. Ocular
gladular tularemia terjadi bila jar.terinfeksi atau
droplet mengenai konjuctiva. Pada semua kasus
terdapat demam, malaise, sakit kepala, nyeri yg
melibatkan kel. Limpe regional

Francisella tularensis
Diagnosis :

- Melalui serologis, dgn pemeriksaan sepasang serum dalam

2 mgg yg menunjukkan adanya peningkatan titer
aglutinasi. Single serum 1/160 diagnosis pasti bila ada
history dan pemeriksaan fisik sesuai dgn diagnosa

Terapi :

- Streptomisin, gentamisin utk 10 hari, tetrasiklin efektif

tapi dpt relaps

Pencegahan :

- Pekerja labor dpt divaksinasi dgn memberi liveattenuated F. tuarensis

Yersinia
Merupakan bakteri batang pendek,
pleomorf, Gram (-), bipolar staining,
catalase (+). Oxidase (-),
mikroerofilik/facultatif anaerob.
Host alami adalah hewan (primer) tp dpt
menyebabkan infeksi serius pada manusia
Spesiesnya : Y.pestis penyebab Plague,
Y.pseudotuberculosis dan Y.enterocolitis
penyebab diare pada manusia

Yersinia

Yersinia pestis dan Plague

Plague adalah infeksi pada rodent, dan dapat ditularkan ke rodent

lain atau kadang-kadang manusia oleh gigitan fleas.
Infeksi yang serius menyebabkan Black Death yang fatal
Morfologi & Identifikasi :
- Batang Gram (-), bipolar staining dgn cat khusus, nonmotil,
facultatif anaerob
- Tumbuh cepat pd media mengandung darah & cairan jar. pd suhu
30OC
- Pada LAD koloni sangat kecil dlm 24 jam
- Inokulum dari bahan yg virulent mempunyai koloni abu-abu,
viscous, tp setelah dikultur di labor berubah jadi koloni irreguler
dan kasar

Struktur antigen

Yersinia

-LPS bersifat endotoxin; -Coagulase (+) pd 28oC tapi tidak pada suhu
35oC; - Menghasilkan bacteriocin (pesticin)
Patogenesis :
Fleas menggigit hewan terinfeksi - m.o. ber-kembang dlm usus.
Krn adanya coagulase terjadi blok pd proventrikulus shg fleas jadi lapar
menggigit sambil mengaspirasi darah kontaminasi luka ok regurgitasi
Y. pestis dari fleas bakteri di fagosit oleh PMN dan Monosit.
Bakteri dalam PMN akan dibunuh sedangkan dalam Monosit akan multiplikasi,
dan mengeluarkan protein antifagosit shg resisten terhadap fagositosis
Bakteri sampai ke kel. Limpe inflamasi hemorrhagik necrosis fluctuant
Bakteri mencapai sirkulasi - sampai pd organ-organ terjadi lesi hemolitik &
necrotik meningitis, pneumonia, serosanguinous pleuro pericarditis
Primer pneumonia terjadi krn inhalasi dari droplet infeksi dari pend. Yg
batuk dengan konsolidasi hemolitik, sepsis dan kematian

Yersinia
Gejala klinik :
-

Inkubasi 2-7 hari, demam tinggi, nyeri lymphadenopathy, pembesaran

kel.limpe, bubo pd lipat paha & axilla, vomitus & diare pd awal sepsis
lalu terjadi penyebaran coagulasi intravasculer terjadi hipotensi,
perubahan status mental, gagal ginjal & jantung, terakhir pneumonia
dan meningitis

Diagnosis Laboratorium
- Bila ada febris pd org yg terekspose rodent dr daerah endemik
suspek Plague
- Spesimen dari : 1) darah (utk kultur), 2) aspirasi kel.limphe (smear &
kultur), 3) Serum fase akut dan konvalensen untuk deteksi antibodi,
sputum dr pend. Pneumonia (kultur), 4) cairan cerebrospinalis pada
meningitis (smear & kultur)

Yersinia
- Smear dilakukan pengecatan dengan Giemsa,
imunofluoresence dan Waysons
- Kultur : LAD. MacConckey dan infusion broth. Kultur sangat
infectious shg perlu hati2
- Serologi : titer antibody 1:16 atau lebih besar diagnosis
atau peningkatan titer
Therapi : Drug of choice Streptomisin, alternatif tetrasiklin,
kadang-kadang kombinasi dengan streptomisin
Epidemiologi : semua pasien ug suspek plague harus diisolasi.
Kontak pend. dgn suspek plague pneumonia harus diberi
tetrasiklin. Vaksin dgn formalin-killied vaccine utk travellers
kedaerah hiperendemi &n org-org yg memp. resiko tinggi

Acute infectious disease maculopapular rash,

fever & resp tract inf.
Pathogenesis & Pathology
- Natural host : human
- Droplet per inhalation primary replication in
resp tract
regional lymphoid tissue viremia :
1. Primary viremia > RES replication
2. Secondary viremia > distant
spreading (skin,
respiratory tract, conjuctiva)
- Spreading can be mediated by lymphocyte.
- Incubation period: 9-11 days to 3 weeks.

Clinical appearance
- Divided into 2 phases :

urine

1. Prodromal phase (2-4 days) : Trias syndromes

> Fever, conjunctivitis, koplik spot
> Isolation : tears, nasal secretion, throat swab,
and blood
2. Eruptive phase (5-7 days) :

> fever decrease centrifugal rash

> Light reddish red, clearly edge, 5-10 days to
become
brownish & desquamation.

Acute infectious disease maculopapular rash,

fever & resp tract inf.
Pathogenesis & Pathology
- Natural host : human
- Droplet per inhalation primary replication in
resp tract
regional lymphoid tissue viremia :
1. Primary viremia > RES replication
2. Secondary viremia > distant
spreading (skin,
respiratory tract, conjuctiva)
- Spreading can be mediated by lymphocyte.
- Incubation period: 9-11 days to 3 weeks.

Clinical appearance
- Divided into 2 phases :

urine

1. Prodromal phase (2-4 days) : Trias syndromes

> Fever, conjunctivitis, koplik spot
> Isolation : tears, nasal secretion, throat swab,
and blood
2. Eruptive phase (5-7 days) :

> fever decrease centrifugal rash

> Light reddish red, clearly edge, 5-10 days to
become
brownish & desquamation.

august 2003
dn

HERPES VIRUSES
1.
1. HERPES
HERPES SIMPLEKS
SIMPLEKS VIRUS
VIRUS TYPE
TYPE 1
1
2.
2. HERPES
HERPES SIMPLEKS
SIMPLEKS VIRUS
VIRUS TYPE
TYPE 2
2
3.
3. VARICELLA
VARICELLA ZOSTER
ZOSTER VIRUS
VIRUS
4.
4. EPSTEIN
EPSTEIN BARR
BARR VIRUS
VIRUS
5.
5. CYTOMEGALO
CYTOMEGALO VIRUS
VIRUS
6.
6. HUMAN
HUMAN HERPES
HERPES VIRUS
VIRUS TYPE
TYPE 6
6
7.
7. HUMAN
HUMAN HERPES
HERPES VIRUS
VIRUS TYPE
TYPE 7
7
8.
8. HUMAN
HUMAN HERPES
HERPES VIRUS
VIRUS TYPE
TYPE 8
8

HERPES VIRUSES
KEY CONCEPS
Mengandung

manusia

bbp patogen yg paling penting pd

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
STRUCTUR DARI HERPES VIRUSES
Morfologi
Morfologi Herpesviruses
Herpesviruses ::

Besar,
Besar, enveloped,
enveloped, mengandung
mengandung genom
genom DNA
DNA
untai
untai ganda
ganda

150
150 200
200 nm
nm

Inti
Inti DNA
DNA dikelilingi
dikelilingi capsid
capsid icosahedral
icosahedral

yg
yg
mengandung
mengandung 162
162 capsomer.
capsomer. Ini
Ini diselubungi
diselubungi oleh
oleh
envelop
envelop yg
yg mengandung
mengandung glycoprotein
glycoprotein

Herpesviruses
Herpesviruses mengkode
mengkode bbp
bbp glyco-protein
glyco-protein utk
utk
perlekatan,
perlekatan, fusion,
fusion, dan
dan menghindar
menghindar dr
dr sistem
sistem
imun
imun

HERPES VIRUSES
CLASSIFICATION FAMILY HERPESVIRIDAE
Subfamily

Virus

Abbreviation

Alphaherpesvirinae

Human herpes virus 1

Herpes simplex type 1
1
Human herpes virus 2
Herpes simplex type 2
2
Human
herpes virus 3
Varicella-zoster virus
Gammaherpesvirinae
Human herpes virus 4
Epstein-Barr virus
EBV
Human herpes virus 8
Kaposis sarcoma
8
Betaherpesvirinae related virus
Human herpes virus 5
Human herpes virus 6
HHV-6
Human herpes virus 7
7

HSVHSVVZV
HHV-

Cytomegalovirus
Herpes lymphotropic virus

CMV

Human herpes virus 7

HHV-

HERPES VIRUSES
TRANSMISSION OF HUMAN HERPES VIRUSES
VIRUS

MEANS OF
TRANSMISSION

HSV-1
HSV-2
VZV

Direct contact
Direct contact
Inhalation,
direct contact
Saliva, blood,
urine ?
Semen ?
Saliva, blood

CMV
EBV
HHV-6
HHV-7
HHV-8

Respiratory,
close contact
?
Saliva

PORTAL OF ENTRY

INITIAL
TARGET CELLS

Mucous membrane, skin

Mucous membrane, skin
Respiratory tract
mucous membranes ?
Blood stream,
mucous membranes
Mucous membranes,
blood stream
?
?
?
?

Epithelial
Epithelial
Epithelial
Neutrophils,
monocytes,
others
B lymphocytes,
salivary glands
T lymphocytes
T lymphocytes
?

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
Ada 2 herpes simplex viruses yg
berbeda :
type 1 & type 2
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 results in latent
infection in the trigeminal
ganglia

Virus resides in latently

infected ganglia in a
nonreplicating state, only
a very few viral genes
arepersistence
expressed in latently
Viral

Genital HSV-2 infection lead

to latently infected sacral
ganglia
Primary infections : usually
mild, in fact most are
asymptomatic (85 90%)

infected ganglia lasts for

the lifetime
More than 80% of the
human population harbor
HSV-1 in latent form,
only a small portion
recurrence

HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
INFECTIONS ASSOCIATED WITH HERPES SIMPLEX VIRUS
Infection Predominant Frequency Age
virus type
group
Ocular herpes

Recurrence

Common

All

Neonatal herpes 2 > 1

Very rare

adults
0 4 weeks

No

MeningoNo
encephalitis
Encephalitis

Un

Developmental
impairment
Adolescence, Resolution

common
Very rare

adults
All

No

Disseminated

1 >2

Rare

All

Oral herpes
Genital herpes
Yes

Usual
outcome

1>2
2>1

Resolution
Yes
visual impairment
Very common All
Resolution
Yes
Common
Adolescence, Resolution

Severe neurologic
impairment
Resolution or

No

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
2

HSV-

Primary or
infection
Primary
Recurrent
infection
recurrent infection
Gingivostomatitis

Cutaneous
Cold
sores, herpes
fever blisters
Pharyngotonsilitis
+
Skin
above
the
waist
Keratitis
Keratoconjunctivitis
Skin below
the waist
Neonatal
infections
Hands or arms
+
Herpetic whitlow
Eczema herpeticum
Genital herpes
Herpes encephalitis
Herpes meningitis

+
+
- +
+-

-+
+

+
+

+
+

HERPES
HERPES SIMPLEX
SIMPLEX VIRUS
VIRUS
CLINICAL FINDINGS
RECURRENT INFECTION

Oropharyngeal disease : cluster of

vesicles, most commonly localized at
the border of the lip, painful, 4 5 days
Keratoconjunctivitis : common &
appear as dendritic keratitis or corneal
ulcers or vesicles on the eyelids
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

VARICELLA-ZOSTER
VARICELLA-ZOSTER VIRUS
VIRUS (VZV)
(VZV)
Varicella (chickenpox) :
a mild, highly contagious disease
chiefly in children
characterized clinically by a
generalized vesicular eruption of the
skin & mucous membranes
The disease may be severe in adults &
immunocompromised children

VARICELLA-ZOSTER
VARICELLA-ZOSTER VIRUS
VIRUS (VZV)
(VZV)

Zoster (shingles)
a

sporadic, incapacitating disease

of
adults or
immunocompromised individuals
characterized by rash limited to
distribution to the skin innervated
by a single sensory ganglion
lesions similar to those of varicella

VARICELLA-ZOSTER
VARICELLA-ZOSTER VIRUS
VIRUS (VZV)
(VZV)
PATHOGENESIS

Varicella : route of infection is the mucosa

of the upper respiratory tract or
conjunctiva
blood

multiple cycle of replication

skin

VARICELLA-ZOSTER
VARICELLA-ZOSTER VIRUS
VIRUS (VZV)
(VZV)

Zoster

skin lesion histopathologicaly identical to

varicella

acute inflammation of the sensory nerve &

ganglia

often only a single ganglion may be

involved

as a rule the distribution of lesions in the

skin corresponds closely to the areas of
innervation from an individual dorsal root
ganglion

Dr.dr. Efrida Warganegara, M.Kes., Sp.MK

INTRODUCTION
The largest & most complex of viruses known
Smallpox first appeared in China and the Far East
at least 2000 years ago.
The family encompasses a large group of agents,
morphologically similar,
share a common nucleoprotein
antigen
The group includes variola virus
etiologic agent of smallpox,
disease has most affected humans
throughout
the world
recorded history until elimination in 1977

POXVIRUSES CAUSING DISEASE IN HUMANS

Genus
host
Orthopoxvirus
extinct)

Vaccinia

Virus

Primary

Variola

smallpox vaccination

Humans

Disease

Humans

Small pox (now

Localized lesion, used

for

Buffalopox Water buffalo Human infection rare, local

Monkeypox
Monkeys
Human infection rare,general
Cowpox
Cows
Human infection rare, local
Parapoxvirus
Orf
Sheep
Human infection rare,
local

Pseudocowpox Cows
Bovine papular Cows
stomatitis
Molluscipoxvirus Molluscum
contagiosum
Yatapoxvirus
Tanapox
local

Yabapox

Monkeys

accidental, localized skin tumor

Milkers nodes

Humans
Monkeys

Many benign skin nodules

Human infection rare,

Human infection very rare,

VIRUS REPLICATION

Comparison of vaccinia & variola virus

:
Vaccinia virus :
Used for smallpox
vaccine
Has a broad host
range
Nucleotide
sequences 192
kb

Variola virus :

Has narow host

range
Nucleotide
sequences 186
kb

PATHOGENESIS & PATHOLOGY OF

SMALLPOX
Portal of entry : mucous membranes
of respiratory tract
1. Primary multiplication in lymphoid
tissue draining the site of entry
2. Transient viremia & infection of RE
cells throughout the body
3. Secondary phase of multiplication
4. Secondary & more intense viremia
5. Clinical disease

Smallpox was transmitted by respiratory

route from lesions in the respiratory tract
of patients in the early stage of the
disease.
During the 12 day incubation period, the
virus was distributed initially to the
internal organs and then to the skin.
Variola major caused severe infections
with 20-50% mortality, variola minor with
<1% mortality.
Management of outbreaks depended on
the isolation of infected individuals and
the vaccination of close contacts.
The vaccine was highly effective. If given
during the incubation period, it either
prevented or reduced the severity of
clinical symptoms.

At least 9 different
poxviruses cause disease
in humans, but variola
virus (VV) and vaccinia
are the best known. VV
strains are divided into
variola major (25-30%
fatalities) and variola
minor (same symptoms
but less than 1% death
rate).
"Variolation" = the
administration of material
from known smallpox
cases (hopefully variola
minor!!!) to protect
recipients - practiced for
at least 1000 years
(Chinese) but risky Jenner was nearly killed
by variolation in 1756!

IMMUNITY
An attack of smallpox complete
protection against re-infection
Vaccination with vaccinia induced
immunity against variola virus at
least 5 years & sometimes longer
Neonates of vaccinated, immune
mother receive maternal antibody
transplacentally, persists for
several months.
After that time, artificial immunity
can be produced by vaccination

Molluscum contagiosum
Molluscum contagiosum
virusis 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
The disease occurs virus
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, fleshcolored, 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.

A.

B.

POSTNATAL RUBELLA (German measles) is a

generally mild, self-limited illness
Characteristic :
Rash
Lymphadenopathia
Low-grade fever
CONGENITAL RUBELLA causes several
anomalia depends on organ defect &
pregnancy age

Symptoms : lymphadenopathy post-auricular,

occipital, lymph nodes cervical posterior, can be
followed by rash or not.
Complete healing without complication
Complication : poly arthralgia, arthritis, encephalitis,
& thrombocytopenic purpura
Asymptomatic re-infection is possible

Infection when pregnant, clinical manifestation

depends on pregnancy age when fetus infected
Probability multiple organ anomaly :
-month II pregnancy : 40 60 %
-Month III pregnancy : 30 35 %
-Month IV pregnancy : 10 %
The ability body defense (cell) immature at
first trimester of pregnancy

Trans-placenta transmission
1. Fetal growth inhibit
2. Cell Chromosome abnormalities
3. death
4. Fetal-mother circulation angiopathy
5. Virus steady at neutralization antibody
6. Disturbance of immune system development
Manifestation
Fetal death, organ anomaly, congenital defect
spontaneous abortion
CD : single/multiple, temporary/permanent

Infant with Congenital Rubella

Diagnosis
*
*

Sign : rash & lymphadenopathy

Laboratory :
1. Serologic : Increase titer of Ig M ELISA,
Nt, HI indirect immuno
fluorescence assay
2. Cell culture: blood, urine, respiratory secr &
CSF immunoperoxydase technique

Detected Ig G from infant blood < 6 months

intrauterine primary infection

Oleh :
Dr.dr.Hj.Efrida Warganegara, M.Kes.,
Sp.MK

BASIC LABORATORY PROCEDURES

Successful isolation of a fungus causing

deseases is dependent upon each of
the following factors :

proper collection of specimen

proper handling and correct
processing of the specimen (including
the inoculation
of the specimen onto
the appropriate
culture medium and
incubation at a
suitable temparature

the expertise of the technologist for

identifying the fungus

Collection of specimens :
1. Skin scrapings :
clean the lesion of dirt or any topical medicines
scrape the outer edge of the lesion with a scalple
collect the scrapings in a clean container
2. Hair : remove hair from the infected site with clean forceps
collect in a clean container
3. Biopsied tissue :
placed in a sterile containers;
add steril water or saline to keep the tissue moist
do not freeze the tissue
4. Exudate or pus :
should be aspirated from an unopened abscess
placed in a steril tube and taken directly to the laboratory
never let the specimen dry

Collection of specimens :
5. Sputum :
collect sputum early in the morning as soon as the
patient awakens
before
brush
thoroughly

collecting the sputum, the patient should

his teeth or remove his dentures, then
rinse his mouth

ask the patient to take a deep cough and raise

sputum
from the lung
collect the sputum in a wide-mouthed, sterile
container that can be tightly closed to prevent leakage
send the specimen directly to the laboratory

Collection of specimens :
6. Blood : should be collected aseptically
placed in the culture medium at the
patients bedside
7. Spinal fluid :
collect aseptically and place into a
sterile
tube
do not refrigerate spinal fluid
8. Urine : collect in asterile container
take directly to the laboratory

Processing of specimens :
Specimens should be processed as soon as
possible :
to ensure that the infecting fungus does not
die
to control contaminating organism
If the specimen cannot be promtly processed, it
should be refrigerated (except spinal fluid).
1. Sputum and bronchial washings :
examine specimen grossly for purulent or
caseous material or particles
prepare smears and wet mounts and
inoculate this material onto appropriate culture
media

Processing of specimens :
2. Spinal fluid, urine and pleural fluid :
concentrate the specimen by centrifugation
make a wet preparation of the sediment and
inoculate
the appropriate media with the remaining
sediment
3. Tissue taken by surgical procedure :
remove any caseous or purulent material and place
onto the appropriate media & prepare wet
preparation
& smears
cut the tissue into small pieces with sterile scissors
and grind the tissue with a sterile mortar and
pestle
transfer the homogenized tissue to appropriate
media

Processing of specimens :
Direct microscopic examination :
is an essential step in diagnosing a fungal
disease
often provide a rapid, tentative diagnosis
(without having
to wait for the culture to
grow)
culture must always be made to correctly
identify the fungus
most mycological specimens are examined in
the fluid state (wet mount), include a KOH
(or NaOH) preparation, India ink. lactophenolcotton blue

Processing of specimens :
Culture media for isolation and identification :
The proper selection of isolation media is critical to
obtaining a laboratory diagnosis of a fungal disease. If the
wrong medium is used, the fungus causing disease may
not grow.
Culture media routinely used may be divided into two main
primary isolation media (non-selective or selective --->
may contain antibiotics to inhibit rapidly growing
fungi)
differential media; are used to identify selected genera
or
or species (by stimulation of characteristic growth /
sporulation; or by the production of physiological
reaction on these media)

Processing of specimens :
Culture media for isolation and identification :
the isolation medium selection depends upon :
the type of specimen (heavily
contaminated,
or
sterile)
the suspected etiological agent
A non selective medium like Sabouraud dextrose
agar
(SDA) should be routinely used
because it will support the growth of almost all
the medically important fungi.
However, without the addition of selective agent
(such as chloramphenicol and
cycloheximide)
this medium is practically
useless.

Processing of specimens :
Temparature of incubation :
is important in the primary
isolation
of fungi
may be room temparature (25 27C) but
prefarably 30C
can act as a selective factor
(incubation at 45C will inhibit most
fungi and bacteria, but not
Aspergillus fumigatus)

Processing of specimes :
Primary isolation media :
non-selective : Sabouraud dextrose agar
Brain heart infusion agar
Blood agar base
selective : Sabouraud dextrose agar with
antibiotics )*
Brain heart infusion agar or antibiotics
and
Blood base agar cycloheximide
)* penicillin, streptomycin or
chloramphenicol

MYCOSES
Superficial mycoses
Cutaneous mycoses
Subcutaneous mycoses
Systemic mycoses :
pathogenic
opportunistic

SUPERFICIAL MYCOSES
Disease

Agent

Pityriasis versicolor
furfur

Malassezia

Pityriasis nigra
hortae

Exophiala

Black piedra

Piedraia hortae

White piedra

Trichosporon
beigelii

PITYRIASIS VERSICOLOR = Tinea versicolor

caused by Malassezia furfur
(Pityrosporum
obiculare) is part of
normal flora of the
skin & scalp ---> the
infections may be
endogenous
the organism is lipophilic, requiring lipid
for growth
Pityriasis versicolor is a chronic, mild,
asymptomatic infection of the stratum
corneum; lesion are sharply
delineated, noninflamatory & cover with
furfuraceous scales

PITYRIASIS VERSICOLOR
the term versicolor is particularly
appropriate, since
color of the lesion
varies according to the normal skin
pigmentation, exposure to sunlight &
severity of infection
lesion occur more often on the upper body,
face, neck, arm
the reason for a change from normal flora
status to
a pathogenic agent are not
clear

PITYRIASIS VERSICOLOR
Laboratory diagnosis :
under uv ligth (Woods lamp) ---> Fluoresence : yellow
wet mount of skin scales : lesion contain short typical
elements & spherical cells (yeast) & this
observation
is virtually pathognomonic (spaghetti &
meat ball
appearance)
culture identification is not diagnostic (may be positive
from noninfective person); but the organism can be
cultured onto SDA (Sabouraud dextrose agar)
covered
with olive oil
Treatment : selenium sulfide, sodium thiosulfate,
miconazole; but recurrent is frequent.

CUTANEUS MYCOSES

may be dermatophytosis, caused by dermatophytes

(Trichophyton, Microsporum, Epidermophyton); or
candidiasis, caused by Candida sp.

Dermatophytosis :
may involve the skin, hair, nails (parts of the body which
contain keratin)
may be acquired from animal (zoophilic), soil (geophilic), in
which lesion are quite inflammatory & may heal
spontaneously
may be acquired from human (anthropophilic); usually less
inflamation but may be chronic
dermatophytosis are classified by the area of the body
involved

DERMATOPHYTES
Antrophophilic

Zoophilic

Geophilic

E.floccosum
M.canis
M.gypseum
M.audouinii
M.nanum
M.fulvum
T.rubrum
T.verrucosum
T.ajelloi
T.schonleini
T.equinum
T.terrestre
T.tonsurans
M.gallinae
T.violaceum
T.mentagrophytes
T.frrugineum
var mentagrophytes
T.concentricum
T.mentagrophytes var interdigitale

DERMATOPHYTES
Tinea capitis (ringworm of the scalp) :
is an infection of the skin and hair of the
head
Clinical features :
graypathes ringworm/epidemic tinea capitis
blackdot ringworm
kerion / zoophilic (geophilic) tinea capitis

DERMATOPHYTES
Tinea Capitis
Grapatches ringworm :

occurs in children & is anthrophilic

is caused by M.audouinii (Europe) & M.ferrugineum (Asia)
is usually non-inflammatory; produced gray pathes of
hair; the hair shaft breakage above the scalp
is contagious through head bands, hats and so on; can
be epidemic in schools; may heal spontaneously at
puberty (prapubertal tinea capitis)
is treated with oral griseofulvin; topical fungistatic
agent such as boric acid

DERMATOPHYTES

Blackdot ringworm :
caused by T.tonsurans; occurs in adults & is a chronic infection
characterized by hair breakage, leaving follicles with dark conidia
(the hair shaft breakage right on the surface of the scalp);
may be results in alopecia; usually treated with griseofulvin or
ketoconazol
Kerion :
occurs primarily in children; usually transmitted by pets;
accordingly by farm animals
is most commonly caused by M.canis or T.mentagrophytes; more
inflammatory & occurs with kerion
may results in inflammation, keloid, kerion, & alopecia
my heal spontaneously; but usually treated with antifungal

DERMATOPHYTES
TINEA FAVOSA (FAVUS)
is caused by T.schonleini; occurs in both childrens & adults
is a severe form, with scutula formation & permanent
hairloss cause by scarring & it has a mousy odor
is treated with griseofulfin & by removal of debris

TINEA BARBAE :
is an acute or chronic folliculitis of the beard, neck or face
is most commonly cause by zoophilic dematophytes
(T.verrucosum; T.mentagrophytes)
results in pustular; or dry, scally lesion; my be
superinfected with bacteria; treated with griseofulvin

DERMATOPHYTES
TINEA CORPORIS :
is fungal infection of the glabrous skin; most commonly caused
by T.rubrum, T.mentagrophytes & M.canis
is characterized by annular lesion with active border & may be
vesicular or pustular
is treated with topical antifungal (tolnaftate, myconazol) or
griseofulvin (systemic)
TINEA IMBRICATA
is caused by T.concentricum; occurs on Pacific Ocean Islands &
numerous countries of Asia
is characterized by concentric ring on the skin; may cover large
area of the body; the scally often overlap
is treated by griseofulvin

DERMATOPHYTES

TINEA CRURIS = Jock itch

is an accute or chronic fungal infection of the groin
is caused by E.floccosum, T.rubrum, T.mentagrophytes,
has some predisposing factors such as : hyperhidrosis,
obesity, diabetes, pregnancy, fluor albus, neurodermatitis
is treated with tolnaftate, miconazol, ketoconazol
TINEA PEDIS = Athlete foot
is an acute or chronic fungal infections of the feet; most
commonly caused by T.rubrum, T.mentagrophytes,
E.floccosum
may be superinfected with bacteria, which may require
antibiotic treatment before tinea pedis is treated

DERMATOPHYTES
TINEA PEDIS
Clinical features : Chronic intertriginous tine pedis :
results in white mascerated tissue bet ween the toes
(the most common form)
is treated with tolnaftate or imidazole & by keeping the
feet dry (by using alumunium chroride) & aerated; if
infections persist, griseofulvin or ketoconazole is used.
Clinical features : chronic dry scally tinea pedis :
results in hyperkeratotic scales on the heel, sole, or
side of the feet; also known as mocasin foot
is treated with hyperkeratotic agent such as whitfield
ointment & griseofulvin

DERMATOPHYTES
TINEA PEDIS
Clinical features : vesicular tinea pedis
is characterized by vesicles & vesiculopustules
permanganate or Burrows solution is used to open vesicle;
dermatophytid reactions my occur;
griseofulvin is the treatment of choice
TINEA MANUM :
is chronic, unilateral fungal infection of the hand, caused
by T.rubrum, T.mentagrophytes, E.floccosum
is characterized by diffuse hyperkeratotic; exfoliative,
vesicular;
treatment = tinea pedis

DERMATOPHYTES
TINEA UNGUIUM :

is fungal infections of the nails caused by Dermatophytes (if

the infections cause by non-dermatophytes, its called
Onychomycosis)
almost always all dermatophytes cause tinea unguium & the
most resistant to treatment
the nails becomes opaque & brittle; usually lose luster; then
discolored, thickened, distorted, seperated from its bed,
thinned & broken
treatment : systemic griseofulvin, long-term (a year or more)
topical : K-permanganate 1:4000; phenol; salicylic acid 10%;
iodium 1%; operative : ablatio

DERMATOPHYTES

course of disease

debris

pain

thickness

Tinea unguium
(Dermatophytes)

Onychomycosis
(Candida sp.)

distal proximal

proximal distal

+
non
+

non
+
non

DERMATOPHYTES
Laboratory diagnosis :
a

diagnosis of fungal etiology based on morphology of

individual lesion & their body locations is not always
sufficient (except for tine imbricata)
infections of skin or nails; a scraping is digested in
KOH and examined for the presence of hyphal element
the infections of the hair shatf show arthroconidia
outside the shaft (ectothrix) or inside the hair shaft
(endothrix)
some species that infect hair fluorescence under
Woods lamp

DERMATOPHYTES
Laboartory diagnosis :
species identification requires culture
culture identification is based primarily on the
appearance of the asexual reproductive conidia or the
specific hyphae
while all of these species grow as molds, they have
distinctive features
the reverse of colonies of some species may be
pigmented (red, yellow) and the tops may be fluffy,
velvety; white or pigmented
this characteristics combine with the microscopic
morphology generally permit an identification

SYSTEMIC MYCOSES
SYSTEMIC MYCOSIS : Opportunistic
Disease

Agents

Candidiasis

sp.

Cryptococcosis

neoformans

Candida albicans; Candida

Cryptococcus

Aspergillosis

Aspergillus
fumigatus; Aspergillus sp.

Zygomycosis

Mucor, Rhizopus, Absidia

SYSTEMIC MYCOSES
Pathogenic
Agent

fungus

Opportunistic

dimorphic fungus

non-dimorphic

Port

dentre lung (per inhalation ) lung &

others

Disease
Patients

usually chronic

usually acute

could be healthy patients

usually ill patient

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 :

oral thrush

is

a yeast infectoins of the oral

mucocutaneus membranes

manifest

as white curd-like patches in

the oral cavity

occurs

in premature infants; older

infants being treated with antibiotics,
immunosuppressed patients, long-term
antibiotics & AIDS patients

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

CANDIDIASIS
Clinical features :

Cutaneus candidiasis

involves the nails ( onychomycosis; paronychis ),

skin folds ( intertriginosa ) or groin ( such as
diaper rash )
may be eczematoid or vesicular / pustular; is
predisposed by moist condition

Clinical feature : alimetary tract disease :

is usually an extension of oral thrush & may

include esophagitis & ultimately the entire
gastrintestinal tract

is found in patients with AIDS or other

immunosuppressive disorder, particularly those
patients on long-term antibiotics therapy

CANDIDIASIS
Clinical feature :

Chronic mucocutaneus
candidiasis

is a chronic, often disfiguring, infections of the

epithelial surfaces of the body

is diagnosed microscipically & by the lack of

cell mediated immunity

Clinical feature :

Bronchopulmonary infections

occurs in patient with chronic lung disease; its

usually manifested by persistent cough

CANDIDIASIS
Clinical feature :

Candidemia / blood borne infections

occurs

most commonly in patients with

indwelling catheter; these infections are
manifested by fever, macronodular skin lesion
& endopthalmitis

Clinical feature :

Endocarditis

occurs

in patient who have manipulated or

damaged valves, or in IV drug abusers

Clinical feature :
may

Cerebrospinal infections

occur in compromised patients

CANDIDIASIS

Laboratory diagnosis :

direct microscopic examination : wet mount of the

skin / nail scraping or exudate, demonstration of the
presence of pseudohyphae / hyphae, & yeast in the
tissue

culture : of the specimens on to SDA at room

temperature, Candida will grows as yaest-like colony

C. albicans be identified by :
* germ tube test -- yeast germination in serum at
370C
* culture on corn-meal-agar -- reveals chlamydospres
* culture on Eosin-methylen-blue-agar : reveals
spider colony
* fermentation test of : glucose, lactose, maltose,
sacharose
serologic : high levels of Candida precipitins or
antigens