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
• Infections in or around Hair Follicles
Folliculitis, furnculosis, & carbuncles are localized abscesses either in
or around hair follicles. Staphylococcus aureus is the most etiologic
agent for all three infections.
•Infections in the Keratinized Layers of the Epidermis
Because of their ability to utilize keratin in the cells of the epidermis,
hair & nails, the dermatophyte fungi are significant & well suited
pathogens for this site.
•Infections of the Deeper Layers of the epidermis &the Dermis
Infections of the Subcutaneous Tissues
Abscesses, ulcers & boils. S. aureus is the most common etiologic
agent of subcutaneous abscesses in healthy individuals. Also the
etiologic agent depends on the site of infection
Infections of the Muscle Fascia & Muscles
Necrotizing Fascitis
Progressive Bacterial Synergistic Gangrene
Myositis
Wound Infections
Postoperative Infections
Bites
Burns
Infections Related to Vascular & Neurologic Problems
Sinus Tract & Fistulas
Systemic Infections with Skin Manifestations
Structure of The skin. (a) Hair and nails are accessory structures of the skin. (b)
Skin is composed of the outer epidermis and the deeper dermis. In addition, a
layer of fat cells called the hypodermis lies beneath the dermis (Bauman, 2012)

Hair
Sweat pores
Nails

Skin

Epidermis
Hair shaft

Dermis

Hypodermis
Microbiota
in hair follicle Nerve

Pressure receptor Sweat gland

Hair root Microbiota in sweat gland

Blood vessels
Hair follicles
Oil gland
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 …yes…check the odor
Skin manifestations of systemic infection caused
by bacteria and fungi:
Organism Disease Skin manifestation
Salmonella tiphi Enteric fever ‘Rase spots’ containing bacteria
Salmonella paratyphi B
(S.scholtmuelleri)
Neisseria meningitidis Septicemia., meningitis Petechial or maculapapular lesions containing bacteria

Pseudomonas aeruginosa Septicemia Ecthyma gangrenosum, skin lesion pathognomonic if infected by

this organism
Mycobacterium leprae Hansens diseases (leprosy), The lesions involve the cooler tissue of the body: skin, superficial
Lepromatous, tuberculoid nerves, nose, pharynx, larynx, eyes, and testicles

Treponema pallidum Syphilis Disseminated infectious rash seen in secondary stage of disease, 2-
Treponema pertenue Yaws 3 months other infection
Rickettsia prowazekii Typhus Macular or hemorrhagic rash
Rickettsia rickettsii Spotted fever Macular or hemorrhagic rash
Rickettsia coronii Spotted fevers 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
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)
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) Staphylococcus aureus
Carbuncles
Subcutaneus fat Cellulitis Streptococcus pyogenes
Fascia Necrotizing fascitis Anaerobes and microaerophiles, usually
mixed infections
Muscle Myonecrosis gangrene Clostridium perfringens (and other
Clostridia)
the skin where Acne Propionibacterium acne
sebaceous glands are
most numerous (Hair
follicles, Dermis)
A

C
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
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
DISEASES
 Due to direct effect  Toxin mediated
of organism  Food poisoning
 Local lesions of  toxic shock
skin syndrome
 Deep abscesses  Scalded skin
 Systemic syndrome
infections
Diseases of staphylococcus
Factors predisposing to S. aureus
infections
 Host factors  Pathogen Factors
 Breach in skin
 Chemotaxis defects
 Opsonisation defects
 Neutrophil functional
defects
 Diabetes mellitus
 Presence of foreign
bodies
 Catalase (counteracts
host defences)
 Coagulase
 Hyaluronidase
 Lipases (Imp. in
disseminating infection)
 B lactasamase(ass. With
antibiotic resistance)
 Protein A
 Toxin (sitolitic,
leucosidin, exfolitive
toxin, TSST
Virulency factors
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
 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
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 :EXO-
TOXIN TSST1 (SUPER Ag )
DI U.S.A KASUSNYA
6000/th; .90% DEWASA DI
DALAM DARAH NYA (+)
Ab SST1.
PENANGGULANGAN :
DRAINAGE & ANTISTAPY-
LOCOCCAL CHEMO-
THERAPI
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

 RITTER’S 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
Staphylococcal scalded skin syndrome. Exfoliative toxin, produced by
some strains of Staphylococcus aureus, causes reddened patches of the
epidermis to slough off.
Which patients are most susceptible to exfoliative strains of S. aureus?
Infants, the elderly, and immunosuppressed patients are most
susceptible
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
 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
Streptococcal Skin Infections
(Streptococcus pyogenes)
Property of Bacterial
 Long chain cocci, Gram positive
 Coloniform in Blood Agar smooth with ß 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
 Bacterial…staphylococcus
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 ( butter-fly wing)
Rheumatic fever sebagai
kelanjutan dari infeksi
Streptococcus pyogenus
pd kulit jarang terjadi

Rheumatic fever
kebanyakan terjadi
sbg kelanjutan infeksi
Streptococcus
pyogenus pada
tenggorokan
Erysipelas. What chemicals cause the reddening of
the skin in erysipelas?
DIAGNOSIS

 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
 Gram staining
 Isolasi dan Identifikasi
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
 Cenderung terjadi pada penderita diabetes
 Etiologinya erat hubungannya dengan lokasi infeksi:
 Pada bagian bawah tubuh  kuman dari tinja dan
urin (pada wanita)
 Pada luka gigitan  kuman berasal dari mulut
 Bila terjadi synergisme antar etiologi (kuman aerob
Stapylococcus dll dengan kuman anaerob Infeksi yang
sangat destruktif
Anaerobic Cellulitis
ciri-ciri khasnya: discharge bau, pembengkakan disertai adanya gas
pada bagian bawah jaringan.
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 pyogenes (flesh eating
bacteria)  kematian tinggi.
 Eksisi radical diperlukan untuk mengangkat jaringan
nekrotik
 pemberian antibiotik lokal dan sistemikFasciitis pada
dinding perut berakibat fatal
Necrotizing Faciitis
Dark blisters of necrotizing fasciitis. The disease,as shown here on a
thigh, is commonly produced by so-called flesheating Streptococcus
pyogenes
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
 Blackened dead tissue and
bubbling of bacterial gas
wastes in gas gangrene.

Perhatikan jaringan necrosis dan akumulasi dari gas pada jaringan

Necrose disebabkan oleh α 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 B 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
Pathogen and Virulence Factors

 The most common causes of acne are propionibacteria: small,

Gram-positive, rod-shaped diphtheroids
 Commonly found growing on the skin.
 They are named for the propionic acid that is a by-product of their
fermentation of carbohydrates.
 The species most commonly involved in infections of humans is
Propionibacterium acnes, which causes acne in 85% of afflicted
adolescents and young adults.
 Staphylococcus aureus may also cause acne.
 Propionibacterium typically grows on sebum within the
sebaceous glands of the skin
The development of acne. Which bacterial
pathogen is a common cause of cystic acne?

Pore 1. Normal skin Oily sebum produced by glands

Bacteria reaches the hair follicle and is discharged onto the
Sebum
Sebaceous Hair
skin surface via the pore.
gland follicle

2. Whitehead Inflamed skin swells over the pore

when bacteria infect the hair follicle, causing the
accumulation of colonizing bacteria and sebum.

Blocked
pore
3. Blackhead. Dead and dying bacteria and sebum
form a blockage of the pore.

4. Pustule formation. Severe inflammation of the

hair follicle causes pustule formation and rupture,
Pus
producing cystic acne, which is often resolved by
scar tissue formation.
Pseudomonas aeruginosa
infection

Pseudomonas aeruginosa infection. Bacteria growing under the bandages

produce the green color on this burn victim.What chemical is responsible for
the green color of this infection?
➤ The greenish blue color of Pseudomonas infections is due to pyocyanin
Hansens Disease (Leprosy)
MYCOBACTERIUM

 Aerobic bacilli –non spore forming

non motile
 Cell wall –rich in lipids
 Acid-fast bacilli
 Very slow growing
Mycobacterium – genus
Cell wall
rich for lipids = hydrophobic surface
= resistent for desinfection
= not accepting colour, but if
stained (special procedure – warming sc.Ziehl
Neelsen) they resist to decolorisation by strong acid
= acid resistent, acid fast
MYCOBACTERIA ASSOCIATED
WITH HUMAN DISEASE
Mycobacterium Environmental Reservoir
contaminant
M tuberculosis No Human
M bovis No Human, cattle
M leprae No Human
M kansasii Rarely Water, cattle
M marinum Rarely Fish, water
M scrofulaceum Possibly Soil, water
M avium intracellulare Possibly Soil, water, birds
M ulcerans No Unknown
M fortuitum Yes Soil, water, animals
M chelonae Yes Soil, water, animals
CLASSIFICATION OF MYCOBACTERIA ASSOCIATED WITH
HUMAN DISEASE
Mycobacterium Clinical significance Pigmentation Growth

Unclassified

M Tuberculosis , M bovis, M ulcerans Strict pathogens No No

M leprae Strict pathogen _ _

Runyon Group 1

M marinum , kansasii Usually pathogenic Photochromogens slow

Runyon Group 2

M scrofulaceum Rarely pathogenic Scotochromogens slow

Runyon Group 3

M avium intracellulare Pathogenic in immunocompromised No slow

Runyon Group 3

M fortuitum, M chelonae Rarely pathogenic No ‘rapid’

Introductions
 Hansen’s disease is the clinical name for the more dreadfulsounding
leprosy
 Chronic and infectious
 It is named after Gerhard Hansen (1841–1912), a Norwegian
microbiologist who discovered its bacterial cause in 1873 before
Koch’s discovery of the tubercle bacillus
 More than 10 million cases of leprosy, mainly in Asia
 The bacilli are often found within endothelial cells of blood vessels or
in mononuclear cells
 Bacilli (ground tissue nassal scrapings)  inoculated into footpads of
mice  local granulomatous lessions with limited multiplication of
bacilli
 Inoculated armadilos  extensive lepromatous leprosy  contain a
unique o-diphenoloxidase (enzyme characteristic of leprosy bacilli = M
leprae human tissue)
Signs and Symptoms
 Hansen’s disease has two different manifestations depending on the
immune response of the patient.
 Patients with a strong T cell immune response are able to kill cells
infected with the bacterium, resulting in a nonprogressive form of the
disease called tuberculoid leprosy
 Patients with a weak T cell immune response develop lepromatous
leprosy, in which the bacterium multiplies in skin, mucous membranes,
and nerve cells, gradually destroying tissue and leading to the
progressive loss of facial features, digits (fingers and toes), and other
body structures.
 Development of signs and symptoms is very slow
 incubation may take years before any are evident.
 Death from leprosy is rare and usually results from the infection of leprous
lesions by other pathogens.
Clinical Findings
Tuberculoid Leprosy Lepromatous Leprosy
Patients with a strong T cell immune response Patients with a weak T cell immune response

Benign and non progressive Progressive and malign

Macular skin lesions nodular skin lessions

Positive lepromin skin test Negative lepromin (extract of lepromatous tissue) skin

Regions of the skin that have lost sensation as a result of nerve Slow symmetric nerve involvement
damage are characteristic of this form of leprosy

Severe asymetric nerve involvement of sudden onset with few Continous bacteremia, very infectious
bacilli present in the lasions

Cell mediated immunity is intact and and the skin is infiltrated Cell mediated immunity is deficient and the skin is infiltrated
with T cells with supressor T cells

strong antibody reaction, defect of cell immunity to M.leprae as strong hypersensitivity of delayed type, feeble humoral
antigen.Many bacteria in skin macrophages (Schwann cells), immunity, many lymphocytes and granulomas, few bacteria in
tissue (activated macrophages fagocyte and eliminated bacteriae

Systemic manifestations: anemia, liphadenopathy, Systemic manifestations: anemia, liphadenopathy,

Eye involvement Eye involvement

Amyloidosis Amyloidosis
Tuberculoid Leprosy
Lepromatous Leprosy
Pathogen and Virulence Factors
 a high G +C
 Non-endospore-forming,
 Gram-positive bacillus with a cell wall containing a large
amount of mycolic acid, a waxy lipid composed of chains of
60–90 carbon atoms
 Acid fast bacilli
 Strict human pathogens
 Cannot be cultivated in-vitro
 Grows best at 30 C
 Armadillo’s used for obtaining M leprae
 Transmission - ? Air borne
 Low infectivity- prolonged contact required
Pathogen and Virulence Factors
 This unusual cell wall is responsible for several
important characteristics of the bacterium:
 • Slow growth rate (due to the time required to
synthesize numerous molecules of mycolic acid). The
generation time varies from hours to several days.
• Protection from lysis once it is phagocytized.
• Growth within phagocytes.
• Resistance to Gram staining, detergents, many
common antimicrobial drugs, and drying out.
 The acid-fast staining procedure was developed to
differentially stain mycobacteria
Pathogen and Virulence Factors
 The bacterium has never been grown in
cell-free laboratory culture, a fact that
has hindered research and diagnostic
studies.
 The nine-banded armadillo, which has a
normal body temperature of 30°C, is its
only other natural host and has proven
valuable in studies on leprosy and on
the efficacy of leprosy treatments
Typical acid-fast bacilli: singly, in parallel bundles or in globular masses
 are regularly found in scraping from skin or mucous membranes
(particularly in the nasal septum) in lepromatous leprosy.
 Mycobacterium leprae
 Spectrum of clinical presentations
 dependent on host –parasite interactions

Tuberculoid Borderline Borderline

Lepromatous
Tuberculoid lepromatous
The leprosy spectrum according to the Ridley and Jopling
classification

tuberculoid leprosy borderline leprosy lepromatous leprosy

TT BT BB BL LL
BI - - -- 2+,3+ 3+, 4+ 5+, 6+
(1+,2+)

BT = borderline tuberculoid leprosy

BB = mid borderline leprosy
BL = borderrline lepromatous leprosy
BI = bacteriological index
- - = negative
+ = degree of positivity
Diagnosis
 Skin test:
 Testing for loss of sensation
 The sweat and histamine tests :
○ Loss of sweating in hypopigmented leprosy macula
○ The histamine test
 Skin smear: Skin or Nasal mucosa scrapings with scalpel
blade  smeared on a slide  stained by Ziehl
Neelsen/auramine stain to demonstrate acid-fast rods:
 LL  numerous
 TT  few, if any organisms are seen  the appearance of
granulomas
 Biopsy of skin  idem point 2
 No serologic test