Titiek Djannatun

Department of Microbiology, Faculty of Medicine

-YARSI University

Infection of The Skin

The flora normal of the skin play an

important role in defending the surface from
foreign invaders
The structure of the skin helps in
understanding the different sort of infection
to which the skin and its underlying tissues
are prone

Three lines of Microbial Attack to The

Skin

Breach of intact skin, allowing infection

from the outside
Skin manifestations of systemic infection,
which may arise as a result of blood-borne
spread from infected focus to the skin or by
direct extention
Toxin-mediated skin damage due to
production of a microbial toxin at another
site in the body (e.g. Scarlet fever, TSS)

Skin manifestations of systemic infection caused

by bacteria and fungi:
Organism

Disease

Skin manifestation

Salmonella tiphi
Salmonella paratyphi B
(S.scholtmuelleri)

Enteric fever

Rase spots containing bacteria

Neisseria meningitidis

Septicemia., meningitis

Petechial or maculapapular lesions containing bacteria

Pseudomonas aeruginosa

Septicemia

Ecthyma gangrenosum, skin lesion pathognomonic if

infected by this organism

Treponema pallidum
Treponema pertenue

Syphilis
Yaws

Disseminated infectious rash seen in secondary stage of

disease, 2-3 months other infection

Rickettsia prowazekii
Rickettsia rickettsii
Rickettsia coronii

Typhus
Spotted fever
Spotted fevers

Macular or hemorrhagic rash

Macular or hemorrhagic rash
Macular or hemorrhagic rash

Streptococcus pyogenes

Scarlet fever

Erythematous rash caused by erythrogenic toxin

Staphylococcus aureus

Toxic shock syndrome

Rash and descuamation due to toxin

Blastomyces dermatitidis

blastomycosis

Papule or pustule develops into granuloma lessions

containing organisms

Cryptococcus neoformans

Crytococcosis

Papule or pustule, ussually on face or neck

Direct Entry Into Skin of Bacteria and Fungi

Structure involved

Infection

Common Cause

Keratinized epithelium

Ringworm

Dermatophyte fungi (Trichophyton,

epidermophyton and microsporum)

Epidermis

Impetigo

Streptococcus pyogenes and/or

Staphylococcus aureus

Dermis

Erysipelas

Streptococcus pyogenes

Hair follicles

Folliculitis
Boils (furuncles)
Carbuncles

Staphylococcus aureus

Subcutaneus fat

Cellulitis

Streptococcus pyogenes

Fascia

Necrotizing fascitis

Anaerobes and microaerophiles, usually

mixed infections

Muscle

Myonecrosis gangrene

Clostridium perfringens (and other

Clostridia)

So what will you be

looking for?

Physical assessment:
a) inspection
b) palpation
c) percussion
d) auscultation

Observe size, shape, color of the

lesions, and yescheck the odor

Bacterial Infections of Skin, Soft Tissue and

Muscle:

The classification depends upon the layer of skin and soft tissue
involved:
Abscess formation. Boils and carbuncles result of infection and

inflamation of the hair follicles in the skin (folliculitis)

Spreading infections (subcutan).
Impetigo (epidermis) bullous, crusted or pustular eruption of the
skin
Erysipelas (Erythematous inflamation) generally on face, legs or
feet and often accompanied by pain and fever
Necrotizing infections.
Fasciitis The inflamatory response to infection of the soft tissue
bellow the dermis causing disruption of the blood supply
gangrene or myonecrosis associated with ischemia of the muscle
layer (anaerobic organisms gas gangrene)

INTRODUCTION

Staphyloccocci - derived from Greek

stapyle (bunch of grapes)
Gram positive cocci arranged in clusters
Hardy organisms surviving many non
physiologic conditions
Include a major human pathogen and
skin commensals

Morphology
microscopis
Kokus, positif Gram,
tersusun seperti buah anggur

Grouping for Clinical Purposes

1. Coagulase positive Staphylococci

Staphylococcus aureus

2. Coagulase negative Staphylococci

Staphylococcus epidermidis
Staphylococcus saprophyticus

A. Staphylococcus aureus

Major human pathogen

Habitat - part of normal flora in some

humans and animals

Source of organism - can be infected

human host, carrier, fomite or
environment

Natural history of disease

Many neonates, children, adults

-intermittently colonised by S. aureus
Usual sites - skin, nasopharynx,
perineum
Breach in mucosal barriers - can enter
underlying tissue
Characteristic abscesses
Disease due to toxin production

DISEASES

Due to direct effect

of organism
Local lesions of
skin
Deep abscesses
Systemic
infections

Toxin mediated
Food poisoning
toxic shock
syndrome
Scalded skin
syndrome

Factors predisposing to S. aureus

infections

Host factors
Breach in skin
Chemotaxis defects
Opsonisation defects
Neutrophil functional
defects
Diabetes mellitus
Presence of foreign
bodies

Pathogen Factors
Catalase (counteracts

host defences)
Coagulase
Hyaluronidase
Lipases (Imp. in
disseminating infection)
B lactasamase(ass. With
antibiotic resistance)

Virulency factors

Diseases of staphylococcus

Immune response

SKIN LESIONS

Boils
Styes
Furuncles (infection of hair follicle)
Carbancles (infection of several hair follicles)
Wound infections (progressive appearance of
swelling and pain in a surgical wound after
about 2 days from the surgery)
Impetigo (skin lesion with blisters that break
and become covered with crusting exudate)

SKIN LESIONS

Etiologi:
Endogenous may be acquired by self-inoculation from a carrier

site (e.g. Nose)

Exogenous acquired by contact with another person
Pathogen Staphylococcus most methicylline and/or vancomycine
resistant

Boils within 2-4 days of inoculation, as superficial infection in

and arround a hair follicle (folliculitis) intense inflamatory
response abscesses, contain abundant yellow creamy pus
Tretment involved drainage and antimicroba (depend on the results
of sensitivity test) may be given when the infection is severe and
the patient hes fever

Folliculitis

Impetigo is a condition
limited to the epidermis,
with typically yellow,
crusted lesions. It is
commonly caused by
Streptococcus pyogenes
either alone or together with
Staphylococcus aureus

DEEP ABSCESSSES
Can be single or multiple
Breast abscess can occur in 1-3% of
nursing mothers in puerperiem
Can produce mild to severe disease
Other sites - kidney, brain from septic
foci in blood

Systemic Infections

1. With obvious focus

Osteomyelitis, septic arthritis

2. No obvious focus
heart (infective endocarditis)
Brain (brain abscesses)
3. Ass. With predisposing factors
multiple abscesses, septicaemia (IV drug
users)
Staphylococcal pneumonia (Post viral)

B. TOXIN MEDIATED DISEASES

1. Staphylococcal food poisoning

Due to production of entero toxins
heat stable entero toxin acts on gut
produces severe vomiting following a

very short incubation period

Resolves on its own within about 24
hours

2. Toxic shock syndrome

High fever, diarrhoea, shock and

erythematous skin rash which desquamate
Mediated via toxic shock syndrome toxin
10% mortality rate
Described in two groups of patients
ass. With young women using tampones
during menstruation
Described in young children and men

TOXIC SHOCK SYNDROME

* ETIOLOGINYA : S.AUREUS PENGHASIL TOKSIN
* MERUPAKAN INFEKSI SISTEMIK YANG MELIBATKAN MULTIPLE ORGAN SYSTEM
* TANDA KHAS: DEMAM, HYPOTENSI DIFFUSE MACULAR RASH
DESQUAMATION OF THE SKIN (PD TELAPAK KAKI ATAU TANGAN)

PENYEBABNYA :EXOTOXIN TSST1 (SUPER Ag )

DI U.S.A KASUSNYA
6000/th; .90% DEWASA DI
DALAM DARAH NYA (+)
Ab SST1.
PENANGGULANGAN :
DRAINAGE & ANTISTAPYLOCOCCAL CHEMOTHERAPI

3. Scalded skin syndrome

Disease of young children
Mediated through minor
Staphylococcal infection by
epidermolytic toxin producing strains
Mild erythema and blistering of skin
followed by shedding of sheets of
epidermis
Children are otherwise healthy and
most eventually recover

STAPHYLOCOCCAL SCALDED SKIN SYNDROME

RITTERS DISEASE in infant , LYELL DISEASE or TOXIC

EPIDERMAL NECROLYSIS in older children
Toxin causes destruction of the intercellular connections and
separation of the top layer of the epidermis . Large blister are
formed, containing clear fluid, and within 1-2 days the overlying
areas of the skin are lost

Antibiotic sensitivity pattern

Very variable and not predictable

Very imp. In Pt. Management
Mechanisms
1.B lactamase production - plasmid mediated
Has made S. aureus resistant to penicillin group of
antibiotics - 90% of S. aureus (Gp A)
B lactamase stable penicillins (cloxacillin, oxacillin,
methicillin) used
2. Alteration of penicillin binding proteins
(Chromosomal mediated)
Has made S. aureus resistant to B lactamase stable
penicillins
10-20% S. aureus Gp (B) GH Colombo/THP resistant to
all Penicillins and Cephalasporins)

Tested in lab using methicillin

Referred to as methicillin resistant S. aureus
(MRSA)
Emerging problem in the world
In Sri Lanka prevalence varies from 20- 40% in
hospitals
Drug of choice - vancomycin
In Japan emergence of VIRSA(vancomycin
intermediate resistant S. aureus)
No effective antibiotics discovered -We might have
to discover

DIAGNOSIS
1. In all pus forming lesions
Gram stain and culture of pus
2. In all systemic infections
Blood culture
3. In infections of other tissues
Culture of relevant tissue or exudate

2. Staphylococcus epidermidis

Skin commensal
Has predilection for plastic material
Ass. With infection of IV lines, prosthetic
heart valves, shunts
Causes urinary tract infection in
cathetarised patients
Has variable ABS pattern
Treatment should be aided with ABST

3. Stapylococcus saprophyticus
Skin commensal
Imp. Cause of UTI in sexually
active young women
Usually sensitive to wide range of
antibiotics

Streptococcal Skin Infections

(Streptococcus pyogenes)

Property of Bacterial

Long chain cocci, gram positive

Coloniforn in Blood Agar smooth with hemolysis
Sensitive bacitracyn
Hyaluronidase help the organism to spread in tissue,
lymphatic involvement, resulting lymphadenitis and
lymphangitis
Lysogenic strains produce pyrogenic exotoxins
(erytrogenic toxins). As with TSST-1 in S.aureus, are
superantigens with a potent influence on the immune
system.Pyrogenic exotoxin SpeA act on skin blood
vessels to cause the diffuse erythematous rash of scarlet
fever, streptococcal pharyngitis, toxic shock syndrome

Property of Bacterial

Surface proteins antigen (M and T) subdivided (type)

streptococcus associated with skin infection (differ from
the types associated with sore throats)
T Protein play no known role in virulence, and their
function is unknown
M protein virulence factors inhibit opsoninization
and confer bacterium resistant to phagocytosis
Additional factors to the virulence organism lipoteichoat
acid and F protein facilitate binding to epithel cells

Impetigo

Impetigo is a condition limited to the epidermis, with typically yellow,

crusted lesions. It is commonly caused by Streptococcus pyogenes
either alone or together with Staphylococcus aureus

Impetigo

Impetigo

Superficial skin infection

Bacterialstaphylococcus
or streptococcus
Spread w/ direct contact
w/ lesions
Thick, yellow crust
(commonly on the face)

Impetigo
S/S
- one or more pimple-like
lesions surrounded by
reddened skin
- lesions fill w/ pus and
later form a thick crust
- itching
Tx
- Topical or oral ABX

Erysipelas : infeksi oleh Streptococcus pyogenus

melibatkan dermal lymphatic. Batas jelas dari
erythema dan indurasi. Bila infeksi pd muka,
maka bentuk radang seperti kupu-kupu ( butterRheumatic fever sebagai
fly wing)
kelanjutan dari infeksi

Streptococcus pyogenus
pd kulit jarang terjadi

Rheumatic fever
kebanyakan terjadi
sbg kelanjutan infeksi
Streptococcus
pyogenus pada
tenggorokan

Acute Glomerulonephritis

Cauced by M types (M49) Streptococcus pyogenes

Occur more often after skin infection than after
infection of the throat
Characterized by the deposition of immune complexes
on basement membran of glomerulus (role of sterp in
the causation is still unclear
Speciment depend on clinical manifestation:
Impetigo: pus from vesicles Gram stain
Erysipelas: skin culture often negatif, culture of fluid
from the advancing edge of the lession may be
successful

Acute Glomerulonephritis

Penicillin is drug of choise, although

erythromycin or an oral cephalosporin may be
used for penicllin-allergic patients
Severe infection may require hospitalization
Since AGN rarely recurs on subsequent
streptococcal infection, long=term pfofilaxis
with penicillin is not indicated (in contrast
following rheumatic fever)

Cellulitis and Gangrene

Introduction

Cellulitis is an acute spreading infection of the skin that involves

subcutaneus tissues. Extend deeper than erysipelas
Originates either from superficial skin lessions such as boils or
ulcer following trauma
Rarely blood-borne, but it may lead to bacterial invasion of the
bloodstream (infection develops within a few hours or days of
trauma and quickly produce a hot red swollen lession, regional
lymphnodes enlarge) patient suffers malaise, chills and fever
The great mayority are caused by S. pyogenes and S.aureus
(depend also on environmental exposure, e.g. Erysipelothrix
rhusiopathiae butchers; V.vulnificus and V.algynolyticus
fishmongers)

When the focus of infection is in subdermal fat, cellulitis-a severe and

rapidly progressive infection-is the typical presentation. Large blisters
and scabs may also be present on the skin surface

PEMERIKSAAN MIKROBIOLOGI
CELLULITIS

Bahan pemeriksan:
aspirat pada daerah pinggiran lesi
pada bagian trauma (bila ada)
biopsi kulit
darah
Penyebaran penyakit sangat progressif
keberhasilan isolasi patogen dari penderita 25-35%
penyebab utama adalah Streptococcus pyogenus dan
Staphylococcus aureus karena hal-hal tersebut diatas maka
diagnose infeksi hanya dari gambaran klinik sakit
antimikroba pilihan, adalah antimikroba yang dapat
menanggulangi etiologi utama (S.pyogenus & S.aureus)

Anaerobic Cellulitis

Terjadi pad adaerah yang mengalami trauma, pada luka

operasi
Cendrung terjadi pada penderita diabetes
Etiologinya erat hubungannya dengan lokasi infeksi:
Pada bagian bawah tubuh kuman dari tinja dan
urin (pd wanita)
Pada luka gigitan kuman berasal dari mulut
Bila terjadi synergisme antar etiologi (kuman aerob
Stapylococcus dll dengan kuman anaerob Infeksi yg
sangat destruktif

Anaerobic Cellulitis
ciri-ciri

khasnya: discharge bau, pembengkakan disertai adanya gas

bagian bawah jaringan.

pada

Diabetic ulcers (this one is

necrotic tissue)

Diabetic Ulcers
Sores on feet, especially on
diabetic patients
Why?
Where?
- areas subjected to weight
bearing
- heel
- tips of most prominent toes

Diabetic Ulcers

S/S
- painful, red sore on foot
- pus when infected
- foul-smelling discharge

Tx
- sterile cleaning, dressings
- refer to diabetic
specialist/surgeon for
debridement or amputation

Necrotizing Faciitis

Merupakan infeksi yg akut dan fatal, etiologinya campuran

dari kuman anaerob dan kuman fakultatif anaerob
infeksi yg sangat toksik, menyebabkan nekrosis berat yang
menyebar ke jaringan sekitar dan bawahnya.
Etiologi utamanya Streptococcus pyogenus (flesh eating
bacteria) kematian tinggi.
Eksisi radical diperlukan untuk mengangkat jaringan
nekrotik
pembrian antibiotik lokal dan sistemikFasciitis pada dinding
perut berakibat fatal

Necrotizing Faciitis

Traumatic Or Surgical Wounds Infected By

Clostridia

Etiologinya, senergitik antara kuman flora normal kulit dengan :

Clostridium tetani tetanus
C.tetani tidak bersifat invasif, Toksin (tetanospasmin) ke otak timbul
gejala tetanus
jalur yg dilalui toksin untuk sampai ke otak:
luka syaraf perifer sitem syaraf pusat (ascending tetanus) di
dalam tubuh penderita masih terdapat Ab terhadap toksi tetani; mudah
ditanggulangi (pemberian anti-toksin secara lokal )
luka darah/ getah bening sistem syaraf pusat (desending
tetanus)
Sukar ditanggulangi, Antitoksin yg diberikan tidak dapat mengikat
kembali toksin yg telah berikatan dengan jaringan (syaraf)
Sukar ditanggulangi, Antitoksin yg diberikan tidak dapat mengikat
kembali toksin yg telah berikatan dengan jaringan (syaraf)

Toksin yang telah

berikatan dengan
syaraf tidak dapat
dinetralkan oleh
antitoksin

Traumatic or Surgical Wounds Infected

infeksi synergistik antara Histotoxic Clostridia dan kuman

fakultatif anaerob (flora normal tubuh &lingkungan)
infeksi bersifat aggressif dan destruktive
tindakan amputasi terpaksa dilakukan guna mencegah penyebaran
toksin ke bagian tubuh lainnya
Yang tergolong dalam Histotoxic Clostridia: C.perfringens (yang
utama), C.histolyticum; C.novyi; C.solderli dll)
Memproduksi aneka ragam toksin dan enzym, memiliki
kemampuan memecah karbohidrat,gunanya untuk mempermudah
invasi kuman dan pembentukan gas pada antar jaringan jaringan
mati membengkak memberi bau khas
sbg isolat dpt ditemukan satu atau lebih kuman Clostridia, dan kuman
fakultatif anaerob lainnya

Perhatikan jaringan necrosis dan akumulasi dari gas pada jaringan

Necrose disebabkan oleh toksin memudahkan infeksi kejaringan sehat lainnya
(jar.pengikat antar sel rusak)
Kumulasi gas sebagai akibat fermentasi (disertai pembentukan gas)& pemecahan
protein oleh Clostridium perfringens dan kuman aerob ikutan lainnya

Perbenihan agar telur

A

A. = + anti-toksin
B. = tanpa anti-toksin

Uji netralisasi toksin NAGLER untuk penentuan type

Clostridium perfringens

Propionibacterium acnes and Acne

Acne terjadi karena kerja sama antara Propinibacteriun acnes dengan

perubahan horman pada masa puber
merupakan infeksi campuran, sebagai isolat selalu ditemukan: kuman
anaerob P.acnes (sebagai etiologi) dan kuman aerob

Mycobacterial Diseases of The Skin

Disebut juga sbg Morbus Hansen (Hansens disease) atau Lepra

Etiologi Mycobacterium leprae
Bentuk batang (+) Gram: tahan asam
Belum dapat dibiak pd perbenihan sintetis
Masa inkubasinya lama (belum ada kesepakatan)
Penyebaran penyakit erat hubungannya dengan sosial ekonomi,
kepadatan penduduk, hygin dll
Gambaran klinik penyakit erat hubungannya dengan Cell Mediated
Immune (CMI) response terhadap M.leprae
Bentuk tuberculoid leprosy (TT) lesi merah, mati rasa, pada
muka, badan kaki dan tangan, dapat sembuh dengan sendirinya
Bentuk lepromateus leprosy (LL), prognosisnya lebih buruk dari
pada (TT)

Mycobacterial Diseases of The Skin