Infections of the Skin - Bacteria

Efrida Warganegara
Introduction
 Normal healthy intact skin protects the
underlying tissues and provides the host
with an excellent defence against invading
microbes.
 In addition to the structural barrier, the skin
is colonized bay an array o organism which
forms its normal flora
 The normal flora of the skin plays an
important roles (as does the normal flora in
other body sites), in defending the surface
from “foreign invaders”
 Introduction
Factors controlling the skin’s microbial load :
- the limited amount of moisture present
- Acid pH of normal skin
- Surface temperature < optimum for many patogens
- Salty sweat
- Excreted chemical such as sebum, fatty acid and urea
- Competition between different species of the normal
flora
Alteration in these factor upsets the ecological balance
of the comensal flora, and predispose to infection
Mode of infection
Microbial disease of the skin may result from any of
three lines of attack :
1. Breach manifestation of intact skin, allowing
infection from the outside
2. Skin manifestation of sysyemic infection; these
may arise as a result of blood-borne spread
from the infected focus to the skin, or by direct
extension as in draining sinuses from
actinomycotic lesion
3. Toxin-mediated skin damage due to production
of a microbial toxin at another site in the body
(scarlet fever, toxic shock syndr.)
 Bacterial infections of Skin, Soft
Tissue and Muscle
These can be classified on an anatomic basis depending on the
layers of skin and soft tissue involved, although some
infection may involve several components of the soft tissues :
1. Abcess formation  Boils and carbuncle are the result of
infection and inflamation of the hair follicle in the skin
(folliculitis)
2. Spreding infection  Impetigo iss limited to the epidermis
and present as a bullous, crusted or pustular eruption of
the skin. Erysipelas involves the dermal lymphatic and
present : erythematous inflamation often accompanied by
pain and fever. If the focus of infection is in the
subcutaneous fat, Cellulitis, a diffuse form of acute
inflamation, is usual presentation
 Bacterial infections of Skin, Soft
Tissue and Muscle
3. Necrotizing infections  Fasciitis describes in
the inflammatory response to infection of the
soft tissue below the dermis. Infection spread,
causing disruption of the blood supply.
-Gangrene or Myonecrosis may follow
infection associated with ischemia of the
muscle layers.
-Gas resulting from the fermentative
metablism anaerobic organism may be
palpable in the tissues (gas gangrene)
Infections of the Skin - Bacteria
Cause : Pyogenic coccus
1. Staphylococcus aureus
2. Streptococcus pyogenes
 1. Staphylococcus aureus
Transmission  by self-innoculation from a
carrier site (nose), or aquired by contact with
an exogenous source, ussually another
person

Virulence Factors 
- one toxin are spesifically related to disease :
Exfoliative toxin with Scalded Skin Syndrome
- Hemolysins, Leucocidin,
Protein A
 1. Staphylococcus aureus
I. Causes PYODERMA (various type of
purulent skin infections): Abscesses,
Furuncles, Sties, Carbuncles, and Impetigo

* Folliculitis (infection of hair follicles) 

furuncle (boils) in the skin; Sties (in the eye
lids)

* Carbuncles, represent a deeper, more

serious condition that result from tunneling,
coalescing abscess
 1. Staphylococcus aureus
* Impetigo (a skin infection found primarily
in children), S.taph aureus alone or with
Strep. pyogenes as coinfectors causes
impetigo
* Impetigo often begins in the nasal area and
spread from there over the face.
* Impetigo is characterized by fragile blisters,
which when broken leave erosions
covered by honey-colored crusts
Diagnosis and Treatment
S. aureus is the most cause of boils and
diagnosis is made on clinical ground.
Gram stain of pus from vesicle in impetigo
show gram pos cocci

Treatment incolves drainage and this is

sufficient for minor lesion but antibiotic may
be given in addition when the infection is
severe and the patient has a fever.
Most S. aureus are beta-lactamase producers
and therefore enzyme-stable penicillins
 1. Staphylococcus aureus
II. Causes SCALDED SKIN SYNDROME (condition
in which there is extensive denuding of the skin).

* It is most often observed in infants and young children

* Syndrome usually begin as erythema araound the

mouth and nose and spread rapidly to affect the skin
of the neck, the trunk, and sometimes the extremities.

* This condition is mediated by an exfoliative toxin of

type A and B

* The disease, seldom fatal because it is limited largely to

the superficial layers nof the skin
1. Staphylococcus aureus
III. Toxic Shock Syndrome
This systemic infection is caused by
S.aureus strain which produce toxic shock
syndrome toxin (TSST)  association
with tampon use by healty women, there
is septicemia, toxaemia and skin
manifestation, include a rash followed by
desquamation of the skin, particularly on
the sole and palmas
 2. Group A Streptococci
(Streptococcus pyogenes)
Virulence Factors :
* Hyaluronic Acid Capsule antiphagocytic
substansice
* Cell Wall Protein (M, R, and T)  The M protein of
the Streptococcal cell wall is the mayor virulence
factor of group A beta-hemolytic streptococci 
inhibits phagocytosis. And now believed to play a
mayor role in the pathogenesis of postinfection
sequelae (e.g Rheumatic fever)
* Extracellular Streptococcal Product (Erythrogenic
Toxin, Hemolysin, Spreading factor/Enzymes : Hyalu-
ronidase, Proteinase, Streptokinase, Nucleases)
2. Group A Streptococci
(Streptococcus pyogenes)

Streptococcal disease is devided into

two categories :

a. The suppurative or primary

infections
b. The non-suppurative or those
infections regarded as complication
following primary infection.
2. Group A Streptococci
(Streptococcus pyogenes)
Suppurative Disease :

- are those in which pus is formed

- One group : often begin as acute
pharyngitis, which can be complicated by
meningitis, OM, pneumonia
- The other groups : include puerperal fever,
as well as such skin infectiona as impetigo,
cellulitis, and erysipelas
2. Group A Streptococci
(Streptococcus pyogenes)
IMPETIGO
- Is a highly contagious skin disease found
primarily.
- The infection begins as small blisters that
can spread to adjacent areas
- The sores become covered with crusts.
- If the infecting strains is nephritogenic, a
streptococcal complication called acute
glomerulonephritis can result
 2. Group A Streptococci
(Streptococcus pyogenes)
CELLULITIS
- Is an inflammatory condition associated with
streptococcal invasion of connective tissue
- Is acute spreading infection of the skin,
extending deeper than erysipelas to involve
subcutaneous tissues
- Infection usually originates either from
superficial skin lesions such as boils or ulcers,
or following trauma.
2. Group A Streptococci
(Streptococcus pyogenes)
It rarely blood-borne but, conversely,
cellulitis made lead to invasion of bacteria
into blood stream.
The great majority of cases of cellulitis are
caused by Strep. pyogenes and Staph.aureus
This type of disease can occasionaly result
with in gangrene with later invasion of
the bloodstream
 2. Group A Streptococci
(Streptococcus pyogenes)

ERYSIPELAS
- Is an infection of the skin or
mucous membrane and is
characterized by spreading
inflammation.
- It is frequently seen on the face
Diagnosis and Treatment
Diagnosis : is usually made on clinical
finding, Gram stain of pus from vesicle in
impetigo show gram pos cocci

Treatment : Penicillin drug of choice 

oral or intramuscular. Erythromycin
should be used for penicilin-allergic
patient
Infections of the Skin - Bacteria
Cause :
1. Clostridium perfringens
2. Propionicacterium acne
3. Mycobacterium leprae
Lain-lain : Gas Gangrene  Clostridium perfringens
 CLOSTRIDIUM GAS-GANGRENE
= Cl. histotoksik
1. Patogen aktif :- Cl. Perfringens
- Cl. Novyi
- Cl. Septicum
- Cl. Histolyticum

2. Non patogen, tapi berbahaya bila ada bersama

golongan I
- Cl. Sporogenes
- Cl. Sordellii
- Cl. Bifermentans
- Cl. tertium
CLOSTRIDIUM PERFRINGENS = Cl. Welchii

SIFAT
 Batang Gram (+), spora (+), oval, sentral
 Tidak anaerob mutlak  dapat tumbuh
bila ada oksigen dg kadar rendah
 Hemolisin (+)
 Memfermentasi glukosa, maltosa, sakarosa
laktosa
 Gelatinase (+), Indol (-), H2S
 5 tipe A - E
 CLOSTRIDIUM PERFRINGENS
* Habitat :
- manusia : C. perfringens merupakan salah satu bagian kecil
dari flora normal fekal pada orang sehat.
- Hewan : Suatu penghuni normal dari isi usus hewan
- Makanan : C. perfringens is ditemukan dalam bermacam-
macam makanan termasuk makanan mentah, dikeringkan
dan dimasak.
- Lingkungan: C. perfringens tersebar luas di tanah, debu
vegetation.

* C. Perfringens dapat menghasilkan (90 %) suatu

infeksi yang invasive, termasuk myonecrosis dan gas
gangrene

* Suatu enterotoksin dari C.perfringens umumnya

menyebabkan keracunan makanan
 CLOSTRIDIUM PERFRINGENS
Toksin
- C.perfringens memproduksi sejumlah besar toksin &
enzim yg menyebabkan infeksi yg menyebar
- Toksin mempunyai sifat : letal, necrotizing, dan
hemolitik
1. Alpha toksin dari C.perfringens tipe A  suatu
lecithinase  letal
2. Tetha toksin  efek mirip, hemolitik &
necrotizing, tapi bukan lecithinase
3. DNase dan Hyaluronidase  suatu kolagenase
yg mencerna kolagen jar.subkutan & otot
 CLOSTRIDIUM PERFRINGENS

4. Enterotoksin (khusus yg tumbuh pd

daging)  menyebabkan diare dalam 6 -
18 jam, karena kerja toksin.
Toksin bekerja dengan cara hipersekresi
di yeyunum & ileum sehingga hilangnya air
& elektrolit dalam diare yang hebat.

Gejala lain nausea, vomitus dan demam.

Penyakit ini mirip dgn penyakit oleh

Bacillus cereus yang cenderung sembuh
sendiri
 CLOSTRIDIUM PERFRINGENS
Patogenesis
- Pada Infeksi  spora mencapai jar. mel.
kontaminasi dr area trauma / dari sal. cerna
- Spora menjadi bentuk vegetatif krn potensial
reduksi-oksidasi yg rendah, sel vegetatif
bermultiplikasi, memfermentasi KH yg ada
dalam jaringan  menghasilkan gas
- Pembengkakan jaringan, mempengaruhi suplai
darah, bersama dengan sekresi toksin
necrotizing dan hyaluronidase  cocok utk
penyebaran infeksi  necrosis jaringan meluas
 kesempatan m.o. utk tumbuh, anemia
hemolitik, dan terjadi toksemia yang berat 
menyebabkan kematian
 CLOSTRIDIUM PERFRINGENS
* Pada Gas Gangrene (clostridial
myonecrosis), infeksi campuran berperan.
Selain clostridia toksigenik, clostridia
proteolitik, bermacam-macam kokus dan
bakteri gram negatif juga ada.
* C.perfringens terdapat dalam sal.kelamin
pada 5% wanita sehingga infeksi uterin
oleh clostrdia sering terjadi mengikuti
aborsi instrumental.
* Clostridia bacteriemia sering terjadi pada
pasien dengan neoplasma.
Gejala klinik
- Dari luka terkontaminasi infeksi menyebar dalam 1-
3 hari dan menghasilkan crepitasi di jar. Subcutan
dan otot, discharge bau busuk, cepat menjadi
necrosis, demam, hemolisis. Toksemia, shock dan
kematian
- Pengobatan  sesegera operasi (amputasi) dan
pemberian antibiotik, sampai diberikan terapi
spesifik. Waktu itu infeksi hanya menghasilkan
fascitis anaerobik dan selulitis
- Keracunan makanan oleh C.perfringens biasanya
terjadi karena makan daging yg mengandung
clostridium. Toksin terbentuk dalam usus dengan
diare yang biasanya tanpa vomitus atau demam pada
6-18 jam. Penyakit berakhir hanya dalam 1-2 hari.
Diagnosis Laboratorium
- Spesimen dari luka, pus dan jaringan

- Adanya sejumlah besar bakteri batang Garam (+) pd

smear menunjukkan adanya clostridium gas gangrene.
Spora tidak selalu ada bila dikultur secara invitro

- Spesimen ditanam pada chopped-meat glukosa agar dan

LAD  inkubasi secara anaerobik  koloni yg tumbuh
dilakukan uji biokimia, hemolisis dan bentuk koloni

- Aktivitas lesitihinase dievaluasi dengan adanya

presipitasi disekitar koloni pada agar egg yolk

- Identifikasi produksi toksin dengan netralisasi oleh

apesifik antitoksin
 PENCEGAHAN DAN PENGOBATAN

 Luka dibersihkan dari kontaminasi

 Jaringan nekrotik dibuang
 Antibiotik
 Hiperbarik oksigen dapat membantu
 Antitoksin tersedia dlm btk
imunoglobulin
 Keracunan makanan oleh enterotoksin
biasanya hanya membutuhkan
pengobatan simptomatik
 Propionibacterium acnes
 Acne : is a common skin disease associated with
young adult.
 Lesion usually encompass benigne whitehead or
blackhead, but also may include deeper
inflamatory lesions.
 If not treated early, the inflamatory lesions can
cause scarring
 Three etiologocal factor in the development of
acne : 1) increased sebum produxction; 2)
hypercornification (dead cells) of follicle
cebaceus ducts -> block; and 3) altered
metabolism of cutaneus microflora (P. acne)
Acne : Propionibacterium acnes
 Mycobacterium leprae
 Organism ditemukan oleh Hansen pada tahun
1873 (9 th sebelum Koch’s menemukan
basil tubercle)
 Tidak dapat dibiak pada media bakteriologi
artifisial (nonliving)
 Basil sering dijumpai dalam sel endotel

pembuluh darah atau sel mononuklear

 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
 Gejala Klinik
- Onset leprosy insidious
- Lesi melibatkan jaringan tubuh yang
dingin : skin, syaraf superficial,
hidung, pharynx, larynx, mata & testis
- 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, bertumpuk-
nya basil tahan asam pd lesi kulit,
bacteriemia terus menerus, test
kulit lepromin negatif
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,

 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 :
 Transmisi paling mungkin terjdi
jika anak kecil terekspose dalam
waktu lama dengan basil yg banyak
 Sekresi Nasal adalah material
infecsius yang paling mungkin bagi
kontak dalam keluarga
 Masa Inkubasi mungkin sekitar 2 –
10 tahun
Mycobacterial diseases of the Skin
Tuberculoid Leprosy
Mycobacterial diseases of the Skin
Lepromatous Leprosy