Chapter 6: Bacterial Infections of Skin

Mar.23.2020 16:00-17:40pm Beijing time

Jan.20.2020

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• Bacterial Infections of Skin is a presentation
for students who have to pass a hard journey to
be a doctor. A lot of clinic photos have been
taken within a long period, and some rare or
complex cases have been merged into this
courseware.
• Some cases in the PPT has not been finally
confirmed, should any mistakes exist there,
please inform me immediately.
• E-mail 386636172@qq.com
Bacterial Infections of Skin

The 2nd Hospital of Yichang

Li Yong
2020-3-23
Key features
• Cutaneous bacterial infections are caused
by resident or transient bacteria in the
epidermis and mucosa. These bacteria
invade the skin where its barrier function is
weak, such as hair follicles, sweat glands
or at the sites of minor trauma.
• The severity of the infection tends to
depend on the relative balance between
the amount and virulence of the bacteria
and the defenses of the host.
 Eczema Wood’s
Lamp

bacteria in plantar skin

increased significantly

Increased bacteria in the foot

skin of eczema patients
• Roughly 20% of outpatient dermatology
visits are for bacterial skin infections.
• Bacterial infections in the skin often have
distinct morphologic characteristics that
should alert the clinician to the fact that a
potentially treatable and reversible
condition exists.
• These cutaneous signs may be an
indication of a generalized systemic
process or simply an isolated superficial
event.
The diagnosis of skin diseases
can be made by the clinical
features in most cases

BCC+Staphyloc
-occus infection
• Pus culture and smear examination may
play definitive roles in diagnosis. Microbial
sensitivity tests need to be performed to
determine the appropriate anti-bacterial
drugs for this bacterium.
• An increase in the prevalence of
community-associated methicillin-resistant
staphylococcus aureus (CA-MRSA) is a
growing concern.
• The development and evolution of
bacterial infection involve three major
factors:
(1) the portal of entry,
(2) the host defenses and inflammatory
response to microbial invasion,
(3) the pathogenic properties of the
organism.
 • Erythrasma— Superficial Cutaneous Infections
• Intertriginous Infections and Intertrigo
• Sec1 Impetigo
Chapter Contents

• Ecthyma
• Sec2 Folliculitis
• Abscess, Furuncle, and Carbuncle
• Sec3 Erysipelas and Cellulitis
• Necrotizing fasciitis
• Sec4 Staphylococcal Scalded Skin Syndrome
• Green Nail Syndrome
• Sec5 Cutaneous Tuberculosis
• Sec6 Leprosy
• Atypical Mycobacteriosis
• Sec7 Erysiploid
Hairless skin Hair skin
 Erythrasma

— Stratum Corneum Infections

• Erythrasma is a chronic bacterial infection
caused by Corynebacterium affecting the
intertriginous areas of the webspace of the
feet, groins, axillae, and submammary
areas, which mimics epidermal
dermatophyte infections.
• The organism rarely causes invasive
infections.
• Age of Onset Adults
• Etiology Corynebacterium, gram-positive ,
part of normal skin flora, which causes
superficial infection under certain
conditions.
• Predisposing Factors Humid cutaneous
micro-climate; warm and/or humid climate
or season; occlusive clothing/shoes;
obesity, hyperhidrosis.
• Symptoms Usually asymptomatic.
Duration: weeks to months to years.
Erythrasma. Hyperkeratosis with a yellowish
hue in the webspace of the foot. The three lateral
webspaces of both feet were involved. The
potassium hydroxide preparation was negative;
Gram stain of the scale shows gram-positive.

Fitzpatrick s Dermatology in General Medicine

Erythrasma: groins (infectious intertrigo). Sharply marginated,
red, slightly scaling appears bright coral-red when examined with
a Wood's lamp. KOH (potassium hydroxide ) preparation was
negative for hyphae.
Erythrasma. Infection of
Corynebacterium. The
diffuse light brown, scaly
plaque resembles tinea in
the axilla. Gram stain of
the scale shows gram-
positive.
Perianal Erythrasma. Well-
demarcated, asymptomatic
erythema and erosion in the
perianal of a 5-year-old boy.
Erythrasma of the vulva may be
misdiagnosis as a candidal
infection. A painful well-marginated
plaque is uniformly red and scaly,
and it has no advancing border.
 Clinical Manifestations
① Macule, sharply marginated.
② Scaling at sites not continuously occluded.
③ In web-spaces of feet, may be macerated, eroded,
or fissured.
④ Often symmetric or in multiple webspaces.
⑤ Red or brownish red; post-inflammatory
hyperpigmentation in more heavily melanized
individuals.
⑥ If pruritic, secondary changes of excoriation,
lichenification.
⑦ Dermatophytosis and/or candidiasis may also be
present.
• Laboratory Examinations
①Wood's Lamp The diagnosis is made by
demonstration of the characteristic coral-red
fluorescence. May not be present if patient has bathed
recently.
②Direct Microscopy Negative for fungal, Gram or
Giemsa stains may show bacterial filaments.
③Bacterial Culture Heavy growth of Corynebacterium.
• Diagnosis Clinical findings, absence of fungi on
direct microscopy, positive Wood's lamp examination.
 coral-red
fluorescence
• Treatment
①Topical antiseptic alcohol gels
②Topical erythromycin or clindamycin solution bid
for 7 days ； mupirocin ointment ， topical
antifungal agents.
③Systemic Antibiotic Therapy Erythromycin or
tetracycline, 250 mg qid for 14 days.
• Sites of Predilection (Intertriginous Areas)
Toe webspaces >groin folds > axillae; also,
intertriginous skin under panniculus, intergluteal,
inframammary.
 Differential Diagnosis, DD
DD • Dermatophytosis
• Intertriginous candidiasis P.50

• Pityriasis versicolor
• Pitted keratolysis
• Inverse-pattern psoriasis P.68
• Seborrheic dermatitis
• Acanthosis nigricans P.70
DD Dermatophytosis Brownish plaques in
the axilla, potassium hydroxide (KOH)
preparation was positive for hyphae.

advancing border no advancing border

DD Adult atopic dermatitis.
lichenification of the neck
and the axillae in a 28-year-
old woman.

Paederus dermatitis
DD

Acanthosis nigricans Pseudoacanthosis nigricans

( liver cancer )
DD

Familial benign pemphigus

DD

Sharply marginated,
brown, slightly scaling
macular patch in the axilla.
Histological diagnosis
Stucco Keratosis.
Integrative skin protect us from
physical injures, chemical injures
& Invasion of pathogens
 Intertriginous Areas
• axillae
• submammary areas (inframammary region )
• periumbilical areas (Umbilicus )
• intergluteal folds
• inguinal folds (groins)
• toe webspaces
• anogenital areas
Diseases in Intertriginous Areas
• Erythrasma
• Intertrigo & Intertriginous Infections
• Dermatophytes, Candida
• Syphilis (Secondary)
• Pemphigus vegetans
• Extramammary Paget’s disease
• Familial Benign Pemphigus
• Acanthosis Nigricans
Intertriginous Infections &
Intertrigo
— Superficial Cutaneous Infections
 Intertrigo
• Intertrigo is a nonspecific inflammation of
opposed skin, occurring in the axillae, groins,
and gluteal folds, submammary areas and
between redundant skin. With increased
moisture and maceration, the stratum corneum
becomes eroded. The problem is common in
obese individuals with
overlapping abdominal folds.
• Intertrigo is diagnosed in the presence of
erythema ± symptoms of pruritus, tenderness, or
increased sensitivity, excluding infectious
causes.
Intertrigo. Chronic lesion with fissure in this obese
patient on the overhanging abdominal fold.
Intertrigo: A tender, light red plaque with a
moist macerated surface extends to the
scrotum and thigh.
Intertrigo. Narrow, well-
demarcated, erythematous
plaque of the intergluteal fold
and perianal area.
Intertrigo of Acanthosis Nigricans
Verrucous proliferation epidermis,
eroded and macerated webspace
moisture and sensitive erythema
 Intertriginous infections
• Intertriginous infections commonly caused by
bacteria (groups A and B streptococcus,
Corynebacterium. minutissimum, Pseudomonas.
aeruginosa) , fungi (dermatophytes, Candida,
and Malassezia furfur) and virus (HPV).
• Dermatoses such as psoriasis inverse pattern,
seborrheic dermatitis, and atopic dermatitis also
occur in body folds, presenting as erythema or
erythematous plaques.
Treatment of Intertrigo
• For acutely symptomatic intertrigo, moist
dressings give immediate symptomatic relief.
Powders with antibacterial/antifungal activity are
helpful for preventing recurrence. In some cases,
zinc oxide ointment reduces friction at involved
sites. Topical glucocorticoid preparations should
be avoided because of the risk of cutaneous
atrophy at these naturally occluded sites. Topical
pimecrolimus and tacrolimus may be effective,
without risk of atrophy.
The webspace is the most common site for erythrasma
in temperate climates. In some cases, interdigital tinea
pedis and/or pseudomonal intertrigo may coexist.
Webspace intertrigo: Pseudomonas aeruginosa
Erosion of a webspace of the foot with a bright red base and
surrounding erythema. Tinea pedis and hyperhidrosis were
also present, which facilitated growth of Pseudomonas
Intertriginous infections: Pseudomonas aeruginosa
 Right groin- Intertrigo

Left groin- Intertriginous infections

Intertrigo and
Intertriginous infections
in 5 days newborn.
Tinea pedis: interdigital macerated type
The webspace between the fourth and fifth
toes is scaling and macerated in a 61-year-
old female. Erythrasma also occurs in the
setting of moist intertriginous sites and may
occur concomitantly with interdigital tinea
pedis and/or Pseudomonas intertrigo.
Webspace Intertriginous infections: Warts
Moisture and maceration facilitate transmition of HPV
Webspace intertrigo / Intertriginous infections of HPV /
Plantar Warts
Candida groin infection.
Tinea cruris usually presents as a
half-moon–shaped plaque that does
not extend onto the scrotum. Candida
groin infections are more extensive
and often bilateral.
They infect the scrotum and show the
typical fringe of scale at the border

s
and satellite pustules.

tule
pus
DD

Cutaneous Atrophy
DD

Familial benign pemphigus

the stratum corneum
became moist and eroded

Perianal Intertrigo aroud genital warts, is one reason of

recurrent of HPV infection.
one week after
operation. Moist dressing
clean discharge of
perianal operating field.
 DD Intertrigo lesion.
oliary erythema
and maceration
Bowen’s disease.
plaque

Perianal intertrigo + Bowen’s disease

Well-demarcated brown plaque, maceration
and erosion in the perianal areas of an 61-
year-old farmer associated with pruritus.
DD Squamous cell carcinoma in situ ,
The cells lost their original arrangement
and were not the same in size
Syphilis (Secondary)
Chronic submammary and
groins lesion with erosions
In a worm-eaten pattern.

P26
DD early stage late stage

Intertrigo
Intertrigo

Lichen sclerosis of the vulva.

There is marked structural change with loss
of the labia minora and midline fusion.
DD Lichen simplex chronicus Chronic rubbing,
scratching result in bilateral erythematous plaques
on vulva, persisting for years.
 DD

Lichenification, most
marked on the left, is the
characteristic finding in
lichen simplex
chronicus. Moist
lichenified skin is generally
hypopigmented.
 P18

Cutaneous candidiasis: Intertriginous infections

Psoriasiform, erythematous lesions becoming confluent on
the vulva with erosions and satellite pustules on the thighs.
Tinea cruris: Intertriginous infections. Confluent,
erythematous, scaling plaques on the medial thighs,
inguinal folds, pubic area and anogenital areas. The
border are slightly raised and sharply marginated.
Erythrasma should be ruled out.
DD

Benign familial chronic pemphigus (Hailey-Hailey disease)

DD

Vitiligo
Cunnus intertrigo: group
A streptococcus.
A painful erythematous
plaque with purulent
exudate in the cunnus and
perianal of a 32-year-
female.
DD

intertriginous dermatitis
DD

Lichen planus.
Well-dermarcated
erythema in the vulva
with fissures and an
extensive white lacy
pattern.
DD Pemphigus vulgaris: Pemphigus vegetans
usually confined to intertriginous regions. Vegetating
granulomatous lesions on anogenital areas.

Intertrigo
Pemphigus Vegetans. An intraepidermal suprabasal cleft
is visible that has resulted from suprabasal acantholysis. It
contains acantholytic and inflammatory cells..

acantholytic
cells
DD Extramammary Paget’s disease
Well-demarcated plaque, maceration
and erosion in the penis and scrotum
DD Extramammary Paget’s disease
Erythematous plaque with hydrated
scale at the base of the scrotum.
DD Extramammary Paget’s disease demarcated
plaque in the perianal areas, maceration and
erosion in anus associated with pruritus.
HE
 pagetoid cells within the epidermis,
EMA （ ++ ）
as a single cells and in nests
 DD
Familial benign pemphigus
This 52-year-old female has had
oozing lesions in both axillae,
submammary regions, inguinal
and periumbilical areas, for
several years. Eruptions worsen
during the summer months. The
mother and two brothers have
similar lesions that wax and wane.
Lesions are painful and show
typical cracks and fissures within
an erosive erythematous plaque.
Although classified among the
blistering diseases, familial benign
pemphigus hardly ever shows
intact vesicles and is often
mistaken for intertrigo.
DD

Familial benign pemphigus

typical cracks and fissures within
an erosive erythematous plaque
DD

Familial benign pemphigus / Hailey–Hailey

disease. Increased moisture and maceration
on anogenital areas.  
DD Psoriasis vulgaris, inverse pattern:
Well-demarcated, erythematous plaque
of the intergluteal fold, perianal area of
a 40-year-old male is only skin
manifestation. So-called inverse pattern
psoriasis occurs in moist intertriginous
sites (skin touching skin): in the axillae,
inframammary region, umbilicus,
intergluteal folds and inguinal folds. It is
commonly mistaken for candidiasis or
tinea corporis, seborrheic and
intertriginous dermatitis.

P18
 inverse pattern psoriasis confluent, erythematous,
DD scaling plaques on the pubic area and scrotum. The
margins are unclear.
 Psoriasis vulgaris erythematous,
DD scaling plaques on the inguinal folds.
DD Malignant acanthosis nigricans. (skin signs of
systemic cancer) starts as a diffuse, velvety
thickening and hyperpigmentation chiefly on the
neck, axillae and other body folds.

P18
2012-4-11
 DD

Malignant acanthosis
nigricans. velvety dark
chocolate-brown plaques in both
axillae of a 72- year-old male with
carcinoma of gastric cardia.

2006-8-4
 Gram­positive coccus infections
• Staphylococci and streptococci cause the
majority of bacterial skin conditions.
• The skin lesions induced by these Gram­positive
coccus appear usually as pustules, furuncles, or
erosions with honey­colored crusts; however,
bullae, widespread erythema and desquamation,
or vegetating pyodermas may also be indicators
of staphylococcus aureus & streptococcus
infection.
 Gram­positive coccus infections
• Staphylococcus aureus and groups A
streptococcus (S. pyogenes) cause superficial
infections of the epidermis (impetigo), which may
extend into the dermis (ecthyma), characterized
by crusted erosions or ulcers. They may arise as
primary infections in minor superficial breaks in
the skin or as secondary infections of preexisting
dermatoses (impetiginization, or secondary
infection).
 r ed ba s e o n
c t io n s i n
The se
t e x t bo o k
your

Section 1 Impetigo

— Superficial Cutaneous Infections

under the horny cell layer
• Age of Onset: Primary infections more common
in children. Secondary infections, any age.
Bullous impetigo: children, young adults.
• Etiology: Staphylococcus aureus most
commonly; also, groups A streptococcus or
mixed staphylococcus aureus and groups A
streptococcus.
• Bullous impetigo 80% caused by staphylococcus
aureus phage group 2 (types 71 and 55), which
produce exfoliative toxins and also cause
staphylococcal scalded-skin syndrome.
1. Bullous Impetigo
• Pathogenesis: Staphylococcus aureus
proliferates in the horny cell layer producing
exfoliative toxin ( ET ) , which leads to
intraepidermal blisters.
• Clinical Manifestations: Vesicles and bullae
containing clear yellow or slightly turbid fluid without
surrounding erythema, arising on normal-appearing
skin. With rupture, bullous lesions decompress. If
roof of bulla is removed, shallow moist erosion
forms.
• Arrangement: more common in intertriginous
sites.
 Bullous impetigo in a child.
Note blisters filled with cloudy
fluid and lesions that have
www.dxy.cn ruptured, leading to erosions
and crusting.
vesicle x 2
In left thigh
flaccid bulla

shallow moist
erosion
Atypical morphologic characteristics
of Bullous impetigo

Only one bulla filled

with cloudy fluid
2. Nonbullous Impetigo
• Clinical Manifestations: Transient superficial
small vesicles or pustules rupture, resulting in
erosions, which in turn become surmounted by a
crust .
• Golden-yellow crusts are often seen in impetigo
but are not pathognomonic lesions; central
healing often apparent if lesions present for
several weeks.
• Arrangement: scattered, discrete lesions;
without therapy, lesions may become confluent;
satellite lesions occur by auto-inoculation.
Nonbullous Impetigo.
Serum and crust at the angle of the
oral cavity and eyelid is a common
presentation for impetigo
Staphylococcal impetigo. Erythema pustules, honey-colored
crusts on perioral of a child with nonbullous impetigo. It can
spread to involve the entire centrofacial region.
Nonbullous impetigo
satellite lesions occur
by auto-inoculation
psoriasis vulgaris Isomorphic phenomenon lichen planus
or Koebner phenomenon

pseudo-isomorphic
phenomenon
 bullous pemphigoid eczema

the distribution
lesion after
of lesions is
scratch
consistent with
the scratch

Isomorphic phenomenon or Koebner phenomenon

psoriasis, bullous pemphigoid, lichen planus, vitiligo, eczema,
Impetigo, warts, molluscum contagiosum, ect.
Diagnosis
• clinical features
• bacterial culture
Treatment
• Topical application of antibiotic ointments and
oral antibiotics are useful.
• Systemic antibiotics are the first line of
treatment.
• A person who has impetigo should be instructed
in proper hygienic techniques to prevent spread
of the infection to others such as keeping the
lesion area dry and not sharing towels before
crusts formation .
Portals of Entry of Infection
① Primary Impetigo Arises at minor breaks in
the skin.
② Secondary Impetigo (Impetiginization)
Arises in a variety of underlying dermatoses
and traumatic breaks in the integrity of the
epidermis.
③ Inflammatory Dermatoses Atopic dermatitis,
stasis dermatitis, psoriasis vulgaris, chronic
cutaneous lupus erythematosus, pyoderma
gangrenosum.
④ Bullous Disease Pemphigus vulgaris, bullous
pemphigoid, sunburn, porphyria cutanea tarda.
Portals of Entry of Infection
④ Ulcers Pressure, stasis.
⑤ Chronic Lymphedema
⑥ Cutaneous Infections Herpes simplex,
varicella, herpes zoster; dermatophytosis (tinea
pedis, tinea capitis).
⑦ Trauma / Wounds Surgical wounds; abrasion;
laceration; puncture; bites(human, animal,
insect); burns; ulcers; umbilical stump.
Differential Diagnosis
• Seborrheic dermatitis
• Atopic dermatitis
• Allergic contact dermatitis
• Epidermal dermatophyte infections
• Tinea capitis
• Herpes simplex ma jo ri ty o f le s io n s w ith
Th e
y -c o lo re d c ru s ts " a re
• Varicella "hone
no t im petigo
• Herpes zoster
• Scabies
• Pediculosis capitis
DD Allergic Contact Dermatitis
Subjective symptoms are intense
pruritus; in severe reactions also
stinging and pain. Staphylococcus
aureus were isolated on culture.
Erythema → papules → vesicles →
erosions → crusts scaling
DD Kaposi's varicella is difficult to
distinguish nonbullous impetigo
Gram stain
shows Gram
positive
 Herpes simplex virus infection: recurrent
DD herpes labialis Grouped and confluent vesicles
with an erythematous rim on the lips and cheek,
2 days after onset of symptoms.

honey-colored crusts
 Herpes zoster.Glistening, honey-colored,
DD delicate crusts around the nose
Herpes simplex and herpes zoster should always
be excluded from non bullous Impetigo
DD Perioral dermatitis A painful well-marginated plaque
is red and scaly.
DD Infective anguler stomatitis
DD

Bullous fixed drug eruption

DD papules, erosions
and crusts at the
hairline on the face

Darier disease is an
autosomal dominant
genodermatosis. The
lesions are prone to
secondary infections with
bacteria, yeast and
dermatophytes.
DD

Secondary Impetigo, Diabetic Bullae: Staphylococcus

aureus. Large bullae arise on the erythema of right foot in 39-
years-old diabetic male.
DD

Acute irritant contact dermatitis, bullea.

following the application of a herbs.
 DD

Pemphigus vulgaris
There are the classic initial lesions:
flaccid, easily ruptured vesicles and
bullae on normal appearing skin.
Ruptured vesicles lead to erosions
that subsequently crust.
 DD

pemphigus vulgaris.
Suprabasilar acantholysis
(separation of epidermal
cells from each other ).
 Ecthyma

— deeper impetigo
• Ecthyma is basically a deeper form of impetigo
caused by staphylococcal or streptococcal ,
nearly always of the shins or dorsal feet. The
disease begins with a vesicle or vesico-pustule,
which enlarges and in a few days becomes
thickly crusted. When the crust is removed there
is a superficial saucer­shaped ulcer with a raw
base and elevated edges .
Ulceration with hemorrhagic crust on the anterior shins
due to infection with group A streptococci
The ulcer has a “punched-out” appearance and
a purulent, necrotic base.
Ecthyma.
Multiple thickly crusted
ulcers on the leg of 40
years old female with
diabetes and renal
failure.
Chronic streptococcal ulcer
 Predisposing Factors
• Ecthyma occurs most commonly on the lower
extremities of children, or neglected elderly
patients, or individuals with diabetes.
• Poor hygiene and neglect are key elements in
pathogenesis.

History
• Duration of Lesions Impetigo: days to weeks.
Ecthyma: weeks to months.
• Symptoms Impetigo: variable pruritus, especially
associated with atopic dermatitis. Ecthyma: pain,
tenderness.
Laboratory Examinations
• Gram Stain Gram positive cocci
• Culture staphylococcus aureus, commonly;
groups A streptococcus (especially from older
lesions). Failure of oral antibiotic may be
indication of infection by MRSA.

Diagnosis
• Clinical findings confirmed by Gram's stain or
culture.
Ecthyma Staphylococcus
aureus. Multiple thickly
crusted ulcers on the leg of a
patient with diabetes.
Ecthymatous lesions were
also present on the abdomen,
and the arms.
Ecthyma Staphylococcus
aureus. Multiple thickly
crusted ulcers on the leg of a
patient with diabetes.
Ecthymatous lesions were
also present on the abdomen,
and the arms.
preexisting dermatoses
is eczema
DD

Venous insufficiency The ulcer with a necrotic base in an

area of stasis dermatitis. Scratch marks indicate itchiness of
surrounding skin, while the ulcers are painful.
 S2 Folliculitis

— inflammation of hair follicle

• Folliculitis is a pyoderma that begins within
the hair follicle.
• Folliculitis is localized inflammation of the
hair follicle caused by infection, chemical
irritation, or physical injury.
• Inflammation may be superficial or deep in
the hair follicle.
Non-infectious causes that need to be considered include
eosinophilic folliculitis, drug-induced folliculitis and irritant folliculitis
 Staphylococcal folliculitis
• One pustule or a group of pustules may appear,
usually without fever or other systemic
symptoms, on any body surface.
• It may occur because of injury, abrasion, or
nearby surgical wounds or draining abscesses.
Etiology and Pathogenesis
• Folliculitis is a pyoderma which originates within
the hair follicle and is ordinarily caused by
Staphylococcus aureus or Staphylococcus
epidermidis.
• It is often secondary to a ①minor trauma,
②obstruction of a hair follicle, ③scratching around
a hair follicle, or ④topical application of
glucocorticoids that allow significant bacterial
multiplication.
Clinical Manifestations
• Staphylococcal folliculitis is a localized bacterial
infection occurring within a single hair follicle.
Pustules occur at a hair follicle openings and are
surrounded by an erythematous halo. Usually,
the crust is formed within several days followed
by healing without scarring in most cases.
• Lesions may be pruritic, tender or painful.
Staphylococcus aureus: Superficial folliculitis.
Multiple pustules confined to the beard area.
── Fitzpatrick s Dermatology in General Medicine
Infectious folliculitis, superficial: S. aureus
Numerous follicular papules and pustules in
the shaved beard area.
 Multiple pustules on neck

Pus culture and smear examination may play

definitive roles in diagnosis
infectious folliculitis,
Follicular pustules are
usually accompanied by an
erythematous rim
Chronic staphylococcal folliculitis on the legs of
scavenger with poor hygiene
On the pubis
staphylococcal folliculitis
may be transmitted
among sexual partners
 Pus culture and smear examination may
play definitive roles in diagnosis

Staphylococcal folliculitis on
the pubis should be differentiated
from herpes simplex virus.
Gram positive cocci can be found
on pus smear.
Diagnosis
• the diagnosis of Staphylococcal folliculitis is
based on the clinical appearance.
• Direct Microscopy ：
①Gram's Stain S. aureus Gram-positive cocci.
②KOH Preparation: hyphae, spores.
• Bacterial culture can confirm the etiology.
Treatment
• Mildest form (only a few eruptions), treatment is
not needed since folliculitis can heal
spontaneously.
• Topical or oral antibiotics are only used in cases
involving multiple eruptions or deeper forms of
folliculitis.
Differential Diagnosis of Staphylococcal folliculitis
• Fungal folliculitis
• Viral folliculitis
• Drug-induced acneform eruptions
• Acne vulgaris
• Perifoliclitis capitis abscedens et suffodiens
• Hidradenitis suppurativa
• Eosinophilic folliculitis of HIV disease
 DD

Fungal folliculitis → furuncle → carbuncle

 DD

2015-5-19

2015-5-30

Tinea capitis_Kerion pain, tenderness,

scaling, diffuse or circumscribed alopecia.
fungal hyphae (+)
2015-6-17
Staphylococcus aureus(+)
 Fungal folliculitis ,
DD Malassezia Folliculitis
Multiple, discrete, follicular
papulopustules on the back,
mimicking acne vulgaris.
Lesional biopsy showed yeast
forms of Malassezia .
The lesions resolved after
treatment with oral itraconazole.

Postop
erative
lung c
ancer
DD Viral folliculitis ,
Follicular

Molluscum contagiosum
is a self-limited epidermal
viral infection, characterized
clinically by skin-colored
papules that are often
umbilicated, occurring in
children and sexually active
adults.
Usually asymptoms, painful
if secondarily infected.
DD Steroid folliculitis

Atrophy

Steroid
Folliculitis

psoriasis
lesion

psoriasis
lesion
 A large number of
pustules spread over the
scalp hair area

Drug-induced
Drug-induced folliculitis.
folliculitis. Acne-like eruption
consisting of papules and pustules but lacking
comedones was seen in a patient who was
receiving Iressa .
DD Occasionally, folliculitis is widespread ,
patients can complain of generalized pruritus.

SLE

Steroid folliculitis
occured 2 weeks after
steroids are started.
lesions appear mainly
on the trunk, shoulders,
and upper arms, with
lesser involvement of
the face.
DD Acne conglobate Acne ?
Folliculitis
?

Acne is an inflammatory of
the pilo-sebaceous units
(pilosebaceous follicles) of
face, trunk, rarely buttocks,
characterized by
comedones, papulopustules,
nodules, cysts and often
scars.
DD
DD
The evolution of a sebaceous follicle (A) to a comedo (B),
to a papulopustule (C), and an inflammatory cyst (D).
Comedo → papulopustule →
inflammatory cyst → Furuncle → Carbuncle
Acne may progress to furuncle or
carbuncle, where the inflammation extends
deeply and involves more than one hair
 DD

Acne inverse with Perifoliclitis

capitis abscedens et suffodiens
 DD
Acne inverse with Perifoliclitis capitis
abscedens et suffodiens
Staphylococcus aureus (+) or (-)
 DD

Eczem
a ？

Infantile acne . Tiny papulopustules on the

cheeks of a 2-week-old newborn.
DD

Acne Fulminans ,
Systemic Acne
 Abscess, Furuncle, and
Carbuncle
— Folliculitis localized inflammation of one
hair follicle
— Furuncle deeper Folliculitis
— Carbuncle several Furuncle
• An abscess is an acute or chronic
localized inflammation, associated with a
collection of pus and tissue destruction.
• A furuncle is an acute, deep-seated, red,
hot, tender nodule or abscess that evolves
from a staphylococcal folliculitis.
• A carbuncle is a deeper infection
composed of interconnecting abscesses
usually arising in several contiguous hair
follicles.
 Abscess
• May arise in any organ or structure. Abscesses
that present on the skin arise in the dermis,
subcutaneous fat, muscle, or a variety of deeper
structures.
• Initially, a tender red nodule forms. In time (days
to weeks), pus collects within a central space.
A well-formed abscess is characterized by
fluctuance of the central portion of the lesion
and can occur at any cutaneous site. At sites
of trauma. Upper trunk for abscesses in
ruptured inclusion cysts. Single or multiple.
Abscess is collection of pus and
tissue destruction. A tender red
erythematous fluctuant abscess
on the corner of lip.
 Furuncle
• Initially, a firm tender nodule, up to 1 ～ 2 cm in
diameter with a central necrotic plug. In many
individuals, furuncles occur in setting of
staphylococcal folliculitis in beard area or neck.
Nodule becomes fluctuant, with abscess
formation below necrotic plug often topped by a
central pustule. After rupture or drainage of
pustule and discharge of necrotic plug, a nodule
with cavitation remains. A variable zone of
cellulitis may surround the furuncle. May arise in
any hair-bearing region: beard area, posterior
neck and scalp, axillae, buttocks. Single or
multiple.
Furuncle an acute, deep-seated,
red, hot, tender nodule on
opisthenar.
Furuncle. Fluctuant erythematous nodule with a
central pustule. 
Labia minora also have hair follicles.
Where there is hair follicle structure, furuncle can be formed
Furuncle
is an acute, deep-seated, red, hot, tender nodule
Furuncle is an abscess that evolves from
a staphylococcal folliculitis
DD Papulopustular rosacea (stage II). Close up
of tiny 1 to 3-mm pustules, often occurring at
the top of the papules.
DD Chilblain classically painful, burning, and/or
pruritic erythematous, papules, deep
nodules, and plaques on the fingers, toes,
and rarely the face. The lesions tend to be
self-limited.
 Carbuncle
• Evolution is similar to that of furuncle.
• Composed of several to multiple, adjacent,
coalescing furuncles .
• Characterized by multiple loculated dermal and
subcutaneous abscesses, superficial pustules,
necrotic plugs, and sieve-like openings draining
pus.
A carbuncle is usually
arising in several
contiguous hair follicles
Carbuncle. Multiple confluent furuncles draining
pus from multiple openings
Carbuncle is a deeper
infection composed of
interconnecting
abscesses.
 Epidemiology and Etiology
• Age of Onset Children, teenager, and young
adults.
• Sex More common in boys.
• Etiology Most commonly MRSA. MRSA
infections becoming more common. Much less
commonly, other organisms.
• Sterile abscess can occur as a foreign body
response (splinter, ruptured inclusion cyst,
injection sites).
Predisposing Factors
– Chronic Staphylococcal aureus carrier state
(nares, axillae, perineum, vagina)
– Diabetes
– Obesity
– Poor hygiene
– Bactericidal defects (e.g., chronic
granulomatous disease)
– Chemotactic defects
– Hyper-IgE syndrome (Job's syndrome)
– HIV disease, especially MRSA infection
Chronic granulomatous disease of childhood
 
Poor hygiene & bactericidal defects
Pathogenesis
• Folliculitis, furuncles, and carbuncles represent
a continuum of severity of Staphylococcal
aureus infection.
• Portal of entry: hair follicle, break in the integrity
of skin.
History
• Duration of Lesions Days to weeks to months.
• Skin Symptoms Throbbing pain and invariably
exquisite tenderness.
• Systemic Symptoms Carbuncles may be
accompanied by low-grade fever and malaise.

Physical Examination
• Skin Lesions are red, hot, and painful / tender.
Laboratory Examinations
• Gram's Stain Gram-positive cocci within leukocytes.
• Bacterial Culture Culture of pus isolates staphylococcus
aureus. Sensitivities to antimicrobial agents may
determine management.
• Antibiotic Sensitivities Identifies methicillin-resistant
staphylococcus aureus (MRSA) and need for changing
usual antibiotic therapy.
• Dermato-pathology Pyogenic infection arising in hair
follicle and extending into deep dermis and subcutaneous
tissue (furuncle) and with loculated abscesses
(carbuncle).
Diagnosis

• Clinical findings confirmed by findings on Gram's

stain and culture.
Differential Diagnosis
Painful Dermal/Subcutaneous Nodule
•Cystic acne
•Tinea capitis_Kerion
•Hidradenitis suppurativa
•Ruptured epidermal inclusion cyst
•Apical dental abscess
•necrotizing lymphangitis
DD Sterile abscess
Ruptured epidermal inclusion cyst
DD
Hidradenitis suppurativa
is a cutaneous disorder that
targets apocrine gland
bearing skin sites, in
sinuse particular the axillae and
anogenital region. It is a
chronic condition
characterized by recurrent
“boils” and draining sinus
tracts with subsequent
scarring.
abscess Draining sinuses over a
fluctuating abscess in the
axilla of a 21-year old man.
This patient also had acne
conglobata.
Hidradenitis suppurativa , buttocks is covered by a
furuncle, multiple openings of sinuses & scars.
DD Hidradenitis suppurativa in the gluteal fold and the
gluteal regions of a 40-year old male. The gluteal fold
is covered by scarring but otherwise relatively little
inflammation is present. There are multiple openings
of sinuses, and pressure releases a serous secretion
as seen on the right buttock.

scar

sinuse
DD

Herpetic whitlow, Herpes simplex virus infection.

Painful, grouped, confluent vesicles on an erythematous
edematous base on the distal finger
trauma 10 days before → S. aureus whitlow
→ pyogenic granuloma
DD Fixed drug eruption, sulfa-nilamide.
DD Panniculitis
DD Idiopathic Calcinosis Cutis

Idiopathic Calcinosis Cutis

A tender red erythematous
fluctuant pseudo-abscess on
the left feet.
DD
Idiopathic Calcinosis Cutis
Treatement _ Furuncles or Carbuncles
• Surgery Incision and drainage are often
adequate for treatment of abscesses, furuncles,
or carbuncles.
• Adjunctive Therapy Application of heat to the
lesion promotes localization / consolidation and
aids early spontaneous drainage.
• Systemic Antimicrobial Treatment speed
resolution in healthy individuals or people at risk
for bacteremia (eg, Immunosuppression).
Carbuncles This lesion
represents multiple confluent
furuncles draining pus from
multiple openings.
Scissors or scalpel blade can be used to drain
loculated pus in carbuncles. All foreign matter must
be removed.
Treatement _ Recurrent Furunculosis
• Recurrent Furunculosis usually related to
persistent S. aureus in the nares, perineum, and
body folds.
• Topical Therapy bar or wash with iodine soap
or benzoyl peroxide. Apply mupirocin ointment
daily to the sites of S. aureus carriage.
• Systemic Therapy Appropriate antibiotic
treatment is continued until all lesions have
resolved. Secondary prophylaxis may be given
once a day for many months.
• Carrier State: Rifampin 600 mg PO for 7 to 10
days for eradication of carrier state.
Furunculosis
recurrent furuncle in earlobe
Recurrent Furunculosis
Usually related to
persistent S. aureus in the
nares, perineum, and
body folds.
S3 Erysipelas and Cellulitis

— Dermal & subdermal infection

Soft-Tissue Infections
• Erysipelas and cellulitis are acute, spreading
infections of dermal and subcutaneous tissues,
characterized by a red, hot, tender area of skin,
often originating at the site of bacterial entry,
caused most frequently by group A streptococcal.
The face & leg is most frequently affected.
• Systemic symptoms such as fever, nausea and
vomiting are commonly present.
• Age of Onset: Any age. Children <3 years; older
individuals.
• Penicillin antibiotics are the first-line treatment
Etiology 1
• Group A streptococci (GAS), Staphylococcus aureus
• Less Commonly
– Group B streptococci (GBS), pneumococci, E. rhusiopathiae
(erysipeloid). In patients with diabetes or impaired immunity: E.
coli, Proteus mirabilis, Acinetobacter, Enterobacter, P.
aeruginosa, Pasteurella multocida, Vibrio vulnificus;
Mycobacterium fortuitum complex, C. neoformans. In children:
pneumococci, N. meningitidis group B (periorbital).
• Opportunistic Pathogens
– Helicobacter cinaedi (HIV disease); C. neoformans; Fusarium,
Proteus, Pseudomonas spp.
• Dog and Cat Bites
– P. multocida and other Pasteurella spp.; S. aureus.
Etiology 2
• Mucocutaneous
–  Underlying dermatoses: Bullous disease (pemphigus vulgaris,
bullous pemphigoid, sunburn); chronic lymphedema;
dermatophytosis (epidermal dermatophytosis/ tinea pedis, tinea
capitis, tinea barbae); viral infections (herpes simplex, varicella,
herpes zoster); inflammatory dermatoses (atopic dermatitis,
contact dermatitis, stasis dermatitis, pyoderma gangrenosum);
superficial pyoderma (impetigo, folliculitis, furunculosis, carbuncle,
ecthyma); ulcers (pressure, chronic venous insufficiency,
ischemic, neuropathic); umbilical stump
–  Trauma: Abrasion; bites (human, animal); insect bites; burns;
laceration; puncture
–  Surgical wound: Surgical incisions; PIC lines
–  Mucosal infection: Oropharynx, nasal mucosa; middle ear
–  Injecting drug use (IDU): "Skin popping" sites
–  Water exposure: V. vulnificus, V. cholerae non-01 and non-0139.
Aeromonas hydrophilia.
Predisposing Factors
• Drug and alcohol abuse, cancer and cancer
chemotherapy, chronic lymphedema
(postmastectomy, postcoronary artery grafting,
previous episode of cellulitis/erysipelas),
cirrhosis, diabetes, nephritic syndrome,
iatrogenic immunosuppression, neutropenia,
immunodeficiency syndromes, malnutrition,
renal failure, systemic atherosclerosis.
History
• Incubation Period Few days.
• Prodrome Malaise, anorexia; fever, chills can
develop rapidly, before cellulitis is apparent
clinically. Higher fever (38.5°C) and chills usually
associated with GAS.
• Immune Status Immunocompromised patients
susceptible to infection with pathogens of low
pathogenicity.
• History Local pain and tenderness. Necrotizing
infections associated with more local pain and
systemic symptoms.
Physical Examination - 01
• Skin Lesions Red, hot, edematous and shiny
plaque, and very tender area of skin of varying
size; borders usually sharply defined, irregular,
and slightly elevated. Vesicles, bullae, erosions,
abscesses, hemorrhage, and necrosis may form
in plaque.
• Lymphangitis. Lymph nodes can be enlarged
and tender, regionally.
Physical Examination - 02
Distribution
• Adults Lower leg; most common site, following
interdigital tinea. Arm: in young male, consider
IV drug use; in female; postmastectomy. Trunk:
operative wound site. Face: following rhinitis,
conjunctivitis.
• Children Cheek, periorbital area, head, neck
Erysipelas of face.
Painful, well-defined,
shiny, erythematous
plaques involving
eyelids, cheeks, and the
nose of an elderly febrile
male. On palpation the
skin is hot and tender.
Portal of entry was
conjunctivitis.
Erysipelas. Painful,
edematous erythema
with sharp margination
on right face. There is
tenderness, fever and
chills.
Erysipelas Erythema
and edema of the left
cheek, associated with
fever and malaise. The
infection is recurrent with
rhinitis (digging nose) as
the portal of entry.
 Erysipelas with
Seborrheic Keratosis
Erysipelas The lower limb is red, hot, tender, and
edematous. Erythematous plaque is well defined. The
infection is recurrent with interdigital tinea pedis as the
portal of entry.
Bullous erysipelas occasionally, blistering may
occur on the edematous erythema.
The lower extremity is swollen, erythematous, and
tender. Both erysipelas & cellulitis can be named by
different docter.
Cellulitis. The acute phase with intense
painful erythema.
Cellulitis, tinea pedis. The extremity is swollen,
erythematous, and tender; there is erosions at
sites of excoriation.
Stasis dermatitis, tinea pedis,
Cellulitis ulcers close to the fascia52
Laboratory Findings
• The elevated ASO and ASK can be used to
indicate streptococcal infection in the patients.
Also the elevated ESR, leukocytosis, and a
positive test of Creactive protein(CRP) can be
observed.
• The detection for causative bacteria may be
difficult from the affected skin sample; however,
it can be confirmed today by PCR detection.
Diagnosis
• the diagnosis of erysipelas is easy according to
the site and the clinical features of the lesions.
• Erysipelas is a superficial cellulitis of the skin.
Cellulitis is more deeply seated than erysipelas,
and its erythematous edges are less clearly
defined. .
• Recurrent erysipelas most cases the eruptions
and fever disappear in about one week; certain
individuaIs have a tendency to develop recurrent
erysipelas on previously affected sites.
Treatment
• Penicillin and Cephalosporins [ˌsefəlɔˈspɔrin]
• Treatment should last 10 days after remission to
avoid recurrence and to prevent complications
from nephritis.
Differential Diagnosis
• Necrotizing fasciitis
• Deep vein thrombophlebitis
• stasis dermatitis
• early contact dermatitis, giant urticaria
• insect bite (hypersensitivity response)
• fixed drug eruption
• erythema nodosum
• acute gout
• prevesicular herpes zoster
• pyoderma gangrenosum
• Sweet's syndrome
 DD

Deep vein thrombo-phlebitis, mostly involving

middle-aged and old women, characterized by
rapid swelling, flushing and fever of lower limb
 Stasis dermatitis ---1/3 of the lower leg is slightly
DD edematous, and the injury or infection near the medial
malleolus forms a long-lasting ulcer
DD

Sweet's syndrome
Sweet’s disease
 Pre-vesicular herpes zoster involving the
DD
second distributions of the fifth cranial nerve.
 herpes zoster Erysipelas Red, hot,
DD
ophthalmicus edematous and shiny
plaque
 Varicella zoster virus
DD infection: Crusted
ulcerations and vesicles on
the right cheek. Marked
facial edema is also
present. Fever, chills and a
culture of group A
streptococcal show
secondary erysipelas or
cellulitis being possible.
 Herpes simplex ophthalmicus, grouped vesicle or
DD
pustuls at muco-cutaneous junctions
 DD

Acute lymphangitis is an inflammatory process involving the

subcutaneous lymphatic channels. Red linear streaks and
palpable lymphatic cords, which may be up to several centimeters
in width, extend from the local lesion toward the regional lymph
nodes, which are usually enlarged and tender.
DD

Cutaneous Signs of Injecting Drug Use (cisplatin):

injection tracks over veins on the dorsum of the hand
Linear tracks with punctures and fibrosis were created by
chemotherapy injections into the superficial veins.
DD

Cutaneous larva migrans (Creeping eruption)

A serpiginous, linear, raised, tunnel-like erythematous lesion
outlining the path of migration of the larva. Upon palpation, it
feels like a thread within the superficial layers of the skin.
 Classification of Wounds
• I. Chronic ulcers
– A. Arterial insufficiency
– B. Venous insufficiency
– C. Neuropathic ulcers/diabetes mellitus
– D. Pressure ulcers (bedsores)
• II. Trauma
• III. Bites Animal, Human
• IV. Surgical wounds
– A. Class I/clean
– B. Class II/clean-contaminated
– C. Class III/contaminated
– D. Class IV/dirty-infected
• Burn wounds
 Necrotizing fasciitis

— Infection involving fascia

• Necrotizing fasciitis is an acute necrotizing
infection involving the fascia.
• It may follow surgery or perforating trauma.
• Within 24 ～ 48h redness, pain, and edema
quickly progress to central patches of dusky blue
discoloration, with or without blisters. Anesthesia
of the involved skin is very characteristic. By the
fourth or fifth day, these purple areas become
gangrenous.
Necrotizing fasciitis
Necrotizing fasciitis
Necrosis of the
subcutaneous fat and
fascia of the inner aspect
of the lower leg in an
elderly patient with
diabetes mellitus.
Right foot stabbed with
iron nail. 
3 maggot found in decaying tissue
Necrotizing fasciitis. The
black necrotic plaque,
resembling a third-degree
burn.
Necrotizing fasciitis
Necrotizing fasciitis
Gastric cancer patients
Cellulitis extends from
the nose to the left
head and face with
extensive necrosis
 Differential Diagnosis
• Vasculitis
• embolism with infarction of skin
• peripheral vascular disease
• purpura fulminans
• warfarin necrosis
• traumatic injury
• fixed drug eruption
• pyoderma gangrenosum
• spider bite
DD

Vasculitis
 Athero-embolism , Cutaneous infarctions with a
DD linear arrangement on the leg of a 79-year-old man
with athero-sclerosis, heart failure, and hypertension.
 Athero-embolism + Cutaneous infarction
DD
3 days after therapy, the infarction and necrosis
progressed slowly.
Necrotic toe in a patient with peripheral arterial obstructive
disease. "Blue toe," "purple toe" syndrome: Acute pain and
tenderness at site of embolization.
DD

initial gangrene
on the great toe
and the 2nd digit Dry
gangrene
 DD

Peripheral arterial obstructive disease. Necrosis present on

lateral aspect of the ankle. This is a female diabetic smoker.
 DD

Stasis dermatitis: large pigmentation, multiple abrasions

and ulcers on the lateral malleolus and dorsum of foot
DD

Necrotizing herpes zoster Confluent,

crusted ulcerations on an inflammatory
base in an elderly male with lungs TB.
 DD

Pressure Ulcers, Stage II: Necrosis,

superficial or partial-thickness involving
the epidermis and/or dermis. Bullae
necrosis of dermis (black) shallow
DD

Spider bites
DD Traumatic injury
DD Pyoderma gangrenosum (PG)
• Pyoderma gangrenosum (PG) is a rapidly
evolving, idiopathic, chronic, and severely
debilitating skin disease. It occurs most commonly
in association with a systemic disease, especially
chronic ulcerative colitis, and is characterized by
the presence of irregular, boggy, blue-red ulcers
with undermined borders surrounding purulent
necrotic bases.
• it does not have a microbial etiology.
Acute onset with painful
hemorrhagic pustule or painful
nodule either de novo or after
minimal trauma.

Repeated treatment with cellulitis, 2006-7-31

necrotizing fasciitis, didn’t improve
Pyoderma gangrenosum. Irregular, boggy, blue-red ulcers
with undermined borders surrounding purulent necrotic bases.
DD

2006-7-31
DD Pyoderma gangrenosum
The clinical presentation of
PG may be diverse and
there is neither a
diagnostic laboratory test
nor pathognomonic
histopathologic findings.
It is therefore important to
avoid misdiagnosing other
diseases.

2006-7-31
S4 Staphylococcal scalded
skin syndrome
— Systemic infection
• Staphylococcal scalded skin syndrome (SSSS)
is also known as staphylococcal toxic epidermal
necrolysis. It is caused by exfoliative toxins
released by Staphylococcus aureus in the
epidermis.
• Age: infants up to age 6.
• A fever and red rash around the mouth or eyes
appear at first, followed by diffuse epidermal
exfoliation with skin tenderness, erosion and
blistering. Nikolsky's sign is positive.
• Systemic management: supportive care,
antibiotics.
Etiology and Pathogenesis
• Staphylococcal scalded skin syndrome is
caused by an exfoliative toxin(ET) produced by
Staphylococcus aureus. The initial infection
occurs commonly at sites such as nasopharynx,
conjunctiva, external ears and umbilicus. The
exfoliative toxin can also affect remote sites via
blood circulation. This toxin is a protease that
targets desmoglein-l (a desmosome structural
protein) leading to epidermolytic effects. As a
result, a pemphigus foliaceus-like acantholysis
and intraepidermal blisters form on the upper
epidermal layer.
Clinical Manifestations - 1
• Staphylococcal scalded-skin syndrome(SSSS)
occurs most frequently in infants and children up
to age 6, it is extremely rare in adults.
• It begins with a red rash and blistering around the
mouth, nostrils, and eye.
• the characteristic facial features: the wrinkles
and fissures around the mouth, nose hole, eye,
discharge and crust .
• The systemic symptoms: fever 38℃ or higher,
irritability, and anorexia .
facial features of SSSS
mucous membranes uninvolved in SSSS
early erythematous areas are very tender

Nikolsky(+)
 Clinical Manifestations - 2
• The erythema begins on the intertriginous areas ,
later the entire skin begins to exfoliate as if
burned, producing erosion. Skin at normal sites
also exfoliates easily by friction (Nikolsky's sign is
positive). Sharp pain is present.
• The mucous membranes tend not to be affected.
• SSSS begins to heal after exfoliation is
accelerated by systemic administration of
antibiotics. Usually, the entire course is 1 to 2
weeks.
SSSS abortive form The erythema begins on the
intertriginous areas , later the entire skin. Skin at
normal sites also exfoliates easily by friction.
SSSS localized form (bullous impetigo)
Intact flaccid purulent bullae, clustered.
Rupture of the bullae results in moist red
and/or crusted erosive lesions.

www.dxy.cn
SSSS generalized form Diffusely erythematous; gentle
pressure to the skin of the trunk has sheared off the
epidermis, which folds like tissue paper.

Nikolsky(+)

www.dxy.cn
Histopathology
• Acantholysis, epidermal clefts and infiltration of
polymorphonuclear cells are observed beneath
the horny cell layer and within the granular cell
layer (the necrolysis is present in upper
epidermis).
• It does not separate at the dermo-epidermal
junction.
large
numbers of
leukocytes

A. Bullous impetigo B. SSSS

In both, cleavage occurs in the granular layer

and is due to acantholysis. large numbers of
leukocytes
Diagnosis
• SSSS can be diagnosed by the characteristic
①facial features
②burn like widespread epidermal exfoliation
③marked Nikolsky's sign (+)
④sparing of the mucous membranes, plams,
soles
Differential Diagnosis
• Most cases of toxic epidermal necrolysis(TEN)
are induced by drugs.
• Histopathologically, the necrolysis of TEN is
present in all epidermal layers and even in
mucous membranes in severe cases.
• Infants are rarely affected by TEN.
• In cases of widely spread multiple bullous
impetigo, the characteristic facial features of
SSSS do not appear and Nikolsky's sign is
negative. ne
egative
?
 Toxic epidermal necrolysis (TEN)
DD are rare, acute and life-threatening
muco-cutaneous diseases . TEN are
nearly always drug-related.

Bullae on the basis

of diffuse erythema.
Nikolsky’s sign(+)
TEN is the most serious drug
eruption. Oral cavity, eye,
respiratory and gastro-intestinal
mucosa can also be involved.
DD

Penicillin induced TEN

 Treatment
• Supportive care : rehydration with intravenous
fluid & antibiotics .
• Local therapy : sterilization , topical application of
ointments that contain antibiotics and petrolatum.
• SSSS tends to have a good prognosis with
proper treatment .
• Systemic management, supportive care, and the
administration of antibiotics are the main
treatments.
Green Nail Syndrome

— Pseudomonas infection
• the nail develops green–black to green–blue
discoloration due to pyocyanin, a blue–green
pigment produced by Pseudomonas aeruginosa.
• Predisposing factors frequent or prolonged
exposure to water, excessive use of detergents
and soaps, nail trauma, other causes of
onycholysis.
• Diagnosis of green nail syndrome is usually
clinical; if necessary, it can be confirmed by Gram
stain (Gram-negative bacillus) and culture of
exudate and nail fragments. The differential
diagnosis includes a subungual hematoma,
melanocytic nevus, melanoma and aspergillus
infection.
Green nail syndrome Tinea Unguium
• Mycobacteria are rod-shaped or coccobacilli
identified by the property of acid-fastness, a
characteristic associated with the composition of
their cell walls.
• Mycobacterial infections are classified as
tuberculosis, leprosy, and infections due to non-
tuberculous mycobacteria (NTM).
• They cause infections in select populations
globally.
S5 Cutaneous Tuberculosis
• Cutaneous tuberculosis ( TB ) is essentially an
invasion of the skin by Mycobacterium
tuberculosis .
• The direct infection of the skin from an outside
source of mycobacteria results in an initial lesion
called true cutaneous tuberculosis.
• Tuberculid is an allergic skin reaction to
Mycobacterium tuberculosis from an
endogenous source .
• Cutaneous tuberculosis is further classified into
subtypes according to the clinical features ,
virulence of the mycobacteria and the immune
response of the patient .
• Most cases of cutaneous tuberculosis have a
history of extra-cutaneous tuberculosis , the
organism reaches the skin via lymphatic or
hematogenous spread. Inoculation cutaneous
tuberculosis does occur.
 Classification of Cutaneous
Tuberculosis
• Exogenous Infection
①Primary inoculation tuberculosis (PIT): via percutaneous
inoculation, occurs at inoculated site in nonimmune host.
②Tuberculosis verrucosa cutis (TVC): via percutaneous
inoculation, occurs at inoculated site in individual with prior
tuberculosis infection.
• Endogenous Spread
①Lupus vulgaris (LV)
②Scrofuloderma (SD)
③Metastatic tuberculosis abscess (MTA)
④Acute miliary tuberculosis (AMT)
⑤Orificial tuberculosis (OT)
• Tuberculosis Due to BCG Immunization
Classification of text book
1 . Cutaneous tuberculosis
1 ) Lupus vulgaris
2 ) Scrofuloderma
3 ) Warty lupus ( Tuberculosis verrucosa cutis)
2 . Tuberculids
1 ) Papulonecrotic tuberculid
2 ) Lichen scrofulosorum
 Cutaneous tuberculosis
50-75% 1 ） Lupus vulgaris
• Lupus vulgaris is the most common type of
cutaneouse tuberculosis.
• It is characterized by small sharply defined
reddish-brown papules appearing on the
face and neck, coalescing into elevated
infiltrative plaques.
Etiology & Pathogenesis(Lupus vulgaris)
• Mycobacterium tuberculosis in extra-cutaneous
organs, transmitted to the skin by blood or
lymphatic vessels.
Lupus vulgaris
A red-brown color painless plaque
covered nose head, scaring in
primary inoculation . Tubercle
bacilli into a tuberculosis-free
individual, and develops at the
site of inoculation.
It occurs chiefly in children and
affects the face or extremities.
A large, elevated and
red-brown plaque of
lupus vulgaris of 7
years' duration involving
the cheek, jaw, and lips.
Clinical Manifestations (Lupus vulgaris)
• A single or severaI, reddish-brown papules first app
ear unilaterally on the face, neck or arm, coalescing
into erythematous plaques. The surface of the plaqu
es exfoliates with scarring in the centers. Papules te
nd to reappear on the scarring areas, and will gradu
ally enlarge and coalesce. This leads to the formatio
n of large firm, elevated plaques in the middle with s
mall reddish yellow or brown nodules on the fringe.
• ulceration and atrophy can occur, or even develop
squamous cell carcinoma.
 web photo

When pressed by a glass slide, the nodules are

yellowish-brown resembling "apple jelly".
 Lupus vulgaris
Reddish-brown plaque, which
on diascopy exhibits the
diagnostic yellow-brown
infiltration apple-jelly color.
Note nodular infiltration of the
earlobe, scaling of right jowl ,
and atrophic scarring in the
lower part of the plaque.

scaling

apple-jelly
scarring
Orificial tuberculosis is a
rare form of tuberculosis.
OT results from
autoinoculation of
mycobacteria from
progressive TB of internal
organ. it is usually found on
the oral, pharyngeal,
vulvar, and anal mucous
membranes.
The pink, scarring plaque
are associated with ulcers
incomplete sinus.
Histopathology (Lupus vulgaris)
• Structure of tuberculoid granulomas: Tube
rcles in the dermis that consists of epitheli
oid cell, with caseous necrosis in the
center and lymphocyte infiltration around.
Langhans giant cells can be found.
Tuberculoid granulomas

Caseous
necrosis

epithelioid
cell Lymphocyte
infiltration
Diagnosis (Lupus vulgaris)
• Lupus vulgaris is diagnosed by the clinical
features, histopathology , and a strong pos
itive for the tuberculin skin test.
• Identification of Mycobacterium
tuberculosis can be done by PCR or cultur
e.
Differential Diagnosis (Lupus vulgaris)
• chronic discoid lupus erythematosus
• cutaneous sarcoidosis
• syphilis 3 stage
• sporotrichosis
DD

Chronic DLE, verrucous hyperplastic plaques

of ear. Lupus band test (+)
DD

DLE, chronic red plaque,

atrophy, ulcer, scab
DD Cutaneous sarcoidosis_
chilblain like lupus type.
Butterfly erythema with
elevated edge.
nodules aggregated to each other
“naked” granulomas
without caseous necrosis

epithelioid
cell

Lymphocyte
infiltration
Langhans
giant cells
DD Cutaneous sarcoidosis _ papule type
DD Cutaneous sarcoidosis _
subcutaneous nodular type
DD sporotrichosis
Treatment (Lupus vulgaris)
• Lupus vulgaris responds well to antituberc
ulous drugs. Although the prognosis is goo
d , it leaves distinct scarring.
 Cutaneous tuberculosis
10 -1 5 % 2 ） Scrofuloderma
1
• Scrofuloderma frequently Involving the neck
and trunk . The lesions begin with painless
subcutaneous nodules that eventually form
fistula (sinus) , and pus Is discharged from
the cold abscesses . It is caused by M .
tuberculosis disseminated from underlying
extracutaneous tuberculosis to the skin .
Cordlike scars develop in most cases .
Clinical Manifestations (Scrofuloderma)
• Scrofuloderma results from direct extension of an e
xisting active TB infection of the lungs , lymph node
s , bones , muscles or tendons .
• A painless light pink subcutaneous nodule called a
cold abscess appears first and becomes softer , gr
adually forming a fistula from which pus is discharg
ed . Later , the ulceration and characteristic cordlik
e scarring develop at a previous scrofuloderma site
,
• Slight localized fever and pain may be seen over th
e course of the disease.
Scrofuloderma in the left neck Scrofuloderma of right neck an
caused by the direct spread of d supraclavicular region, the a
tuberculosis of the lymph bscess formed extensive skin
nodes in the left neck ulcer

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Laboratory Findings (Scrofuloderma)
• Large quantities of Mycobacterium tuberculosis can
be found in the pus and skin tissue samples .
• The presence of mycobacteria can be confirmed by
PCR or culture .

Treatment (Scrofuloderma)

• same as lupus vulgaris .

 Cutaneous tuberculosis
4-5% 3 ） Warty lupus
Etiology and Pathogenesis(Warty lupus)
• Warty lupus is a variant type of cutaneous
tuberculosis .
• The indurated , warty skin lesions arise by
inoculation of tubercle bacilli in an individu
al previously infected with Mycobacterium
tuberculosis , who usually has a moderate
or high degree of immunity to TB.
Clinical Manifestations (Warty lupus)
• Warty lupus occurs most frequently at the ends
of extremities, dorsal surfaces of joints , and butt
ocks , secondary to external stimulation or injury
. Several small , asymptomatic , indurated wart-li
ke papules with a slight inflammatory edge coale
sce and enlarge, forming erythematous verrucou
s plaques at the periphery . The lesions enlarge
centrifugally and tend to heal in the center . Wart
y lupus is an infection of the superficial layers , s
o ulceration is rare.
Lesions progress slowly and, if
untreated, persist for many years.
Spontaneous involution eventually
occurs, leaving an atrophic scar
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Warty lupus of right buttock. An annular granulomatous plaque
with central healling and active fringe.  
Warty
lupus （ Tuberculosis
verrucosa cutis ） occurs
from exogenous inoculation
of bacilli into the skin of a
previously infected person
with strong immunity against
tuberculosis.
The lesions are persistent
more than 8 years , usually
superficial and limited in their
extent.
Histopathology (Warty lupus)
• Histopathology of the epidermis shows hyperker
atosis and parakeratosis with marked acanthosis
and papillomatous proliferation . An inflammatory
infiltration mainly composed of neutrophils acco
mpanied with lymphocytes can also be found in t
he dermis . Abscesses may occasionally occur ,
and tuberculoid structure with caseous necrosis
may be observed.
Diagnosis (Warty lupus)
• Identification of M. tuberculosis can be ma
de by PCR or culture . A strong positive tu
berculin skin test. Histopathology finding.

Differential Diagnosis (Warty lupus)

• Lupus vulgaris , DLE, chromomycosis , vir
al warts , tinea cruris.
 chronic DLE also has verrucous
DD
hyperplastic plaques
Treatment (Warty lupus)
• Warty lupus responds well to antituberculo
us drugs
 Tuberculids
• Tuberculids are skin disorders associated
with an underlying focus of internal tuberc
ulosis . The cutaneous symptoms are thou
ght to be immune reactions in the skin res
ulting from hematogenous dissemination o
f M. tuberculosis or its antigens from a pri
mary infection . Individuals with strong cell
-mediated immunity tuberculosis are easily
affected.
 Tuberculids
1 ) Papulo-necrotic tuberculid
• This is thought to be vasculitis caused by allergic r
eaction to Mycobacterium tuberculosis .
• It occurs in young people , most frequently on the
extens or surfaces of extremities , particularly on t
he elbows hand and knee, Multiple , dark red papu
les with a diameter of l cm or less appear , forming
pustules and ulceration . They heal with scarring .
These eruptions occur continuously and progress
slow presenting new eruptions mixed with old ones
.
• Anti-tuberculous drugs are effective
 ─ ─ 《皮肤结核》孙
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Multiple red papules and pustu

les on the extension side of el
bow and knee and hand.
There is a crater like ulcer on
the top of some lesions,
covered with scab.
 Tuberculids
2 ) Lichen scrofulosorum
• Lichen scrofulosorum most frequently occurs after an initia
l infection of M. tuberculosis or BCG vaccination .
• Red follicular papules , scattered or aggregated , and of I
mm to several millimeters diameter appear on the trunk or
extremItIes . Histopathologically , epithelioid cells , Langha
ns giant cells and granulomas are found in the dermis ; ne
vertheless caseous necrosis Is not present nor is M. tuber
culosis detected . Therefore , lichen scrofulosorum is cons
idered to be tuberculid , an allergic reaction against mycob
acterial compounds .
• Anti-tuberculous drugs and minocycline are useful . Mos
t cases heal in several months.
Lichen scrofulosorum
Rosette like distribution of
trunk and dense distribution of
polygonal and flat top papules
with pigmentation on anterior
─ ─ 《皮肤结核》孙
abdominal wall.
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Lupus miliaris disseminatus
facies. Formerly known as
tuberculosis, there is no
relationship to tuberculosis.
Firm, yellowish­brown or red, 1–3
mm, monomorphous, smooth­
surfaced papules are present on
the butterfly areas, lateral areas,
and mandible. The eyelid skin is
characteristically involved.
Lupus miliaris disseminatus
facies discrete papules appear
as yellowish­brown lesions on
diascopy , correspond to
caseous epithelioid granuloma
histologically. Self-­involution is
expected in several years .
S6 Leprosy
• Leprosy is a chronic granulomatous disease
caused by Mycobacterium leprae, principally
acquired during childhood/young adulthood.
• Skin, peripheral nervous system, upper
respiratory tract, eyes, and testes are the major
sites of involvement.
• Clinical features, natural history, and prognosis
are related to the host's immunologic response
(cell-mediated immunity).
• Etiology Mycobacterium leprae
• Pathogenesis The clinical spectrum of
leprosy depends entirely on variable limitations
in the host‘s capability to develop effective cell-
mediated immunity.
• Epidemiology Because the pathogenicity
of M. leprae is extremely low , the natural
immune response normally eliminates the
infection . The incubation period is about 3 to 5
years . extremely rare , occurs worldwide .
• Classification of Leprosy based on clinical,
immunologic, and bacteriologic findings.
①Number of Mycobacterium leprae
LL﹥BL﹥BB﹥BT﹥TT least
②Cellular immune response
TT﹥BT﹥BB﹥BL﹥LL weakest
 Clinical Manifestations - 01
①Tuberculoid leprosy ( TT ) : mildest form . strong
cellular immunity . Sharply demarcated, locallzed ,
erythematous patches or papules appear either
single or multiple . Faded papules also appear .
Alopecia , reduced sensation & perspiration
②Lepromatous leprosy (LL ) cellular immunodeficiency
. leproma In the peripheral nerves , eyes and lymph
nodes. Multiple nodules on the skin . visual
impairment, neuralgia , deformity of face &
extremities
 Clinical Manifestations - 02
③Borderline leprosy ： borderline tuberculoid leprosy
( BT ) , mid-borderline leprosy ( BB ) , borderline
lepromatous leprosy ( BL ) .
intermediate in severity between TT and LL.
Complex clinical features of TT and LL.
④Indeterminate leprosy ( IL ) easily escapes diagnosis
as leprosy. Two or three flat , poorly demarcated ,
light pink patches appear.Peripheral nerve symptoms
are mild or absent.
Characteristic findings of leprosy are not found in a
skin biopsy .
Tuberculoid leprosy,
TT Well-defined,
hypopigmented, slightly
scaling, anesthetic
macules and plaques on
the posterior trunk.
Mid-borderline
leprosy,BB
Annular tan-pink plaque
on the neck with similar
lesion on the near cheek.
Peripheral sensory
nerves were palpable on
the neck.
Borderline lepromatous
leprosy, BL
Well-demarcated,
infiltrated, erythematous
plaque on the periorbital
region.
The initial diagnosis was
erysipelas, which did not
respond to antibiotic
treatment.
Laboratory Findings
① M. leprae is detected from the tissue fluid and /
or pathological tissue of the lesion by acid-fast
stain . Number of M.leprea LL﹥BL﹥BB﹥ BT
﹥TT
② The lepromin test may be used for classification
of leprosy : positive TT﹥BT﹥BB﹥BL﹥LL
③ PCR

Histopathology
① epithelioid granuloma , Langhans giant cells
surrounded by infiltration of multiple lymphocytes.
② Leprae proliferates in macrophages .
Diagnosis
① skin lesions accompanied by reduced sensation
② thickening of peripheral nerves
③ neurological disorders
④ laboratory findings and histopatholgy.

Differential Diagnosis
tuberculosis , syphilIs , cutaneous mycosis ,
diseases accompanied by peripheral nerve
Impairment (eg.diabetes) , syringomyelia and
cutaneous lymphoma.
Treatment
• dapsone , rifampicin , clofazimine
• 6 months in mild cases , 2 years in severe
cases

① Chronic dermatosis without pruritus

② Undiagnosed skin disease
 Atypical Mycobacteriosis
(Non-tuberculous Mycobacteriosis)
• Atypical (non-tuberculous) mycobacteria exist in
a wide variety of natural sources, such as soil,
water, and animals; most human disease is
acquired from the environment.
• Many of these organisms do not cause infection
and are simply commensals or saprophytes.
 Clinical features
• The initial lesion is a single bluish-red
inflammatory nodule or pustule at the site of
inoculation, which is often on an upper extremity.
It then forms a crusted ulcer, suppurative
abscess or verrucous nodule.
• Multiple lesions can develop along the course of
the draining lymphatics.
 s e 1
C a

Fishing fun exposed to fishing pool are at risk. A papule evolves

into a nodule at the site of trauma 2-3 weeks earlier. The new
nodules invades the arm along the dorsal of right hand.
Case 2

sporotrichoid pattern
The nodules and abscesses are
arranged along the lymphatic vessels.
 Case 3

A sporotrichoid pattern with the inoculation site on dorsum of

hand.
Clinical presentations include pustules, keratotic plaques ,nodules
with or without suppuration, a sporotrichoid pattern, and ulcers
with draining sinuses.
HE x 40

Verrucous proliferation
HE x 100

No granuloma formation
Langerhans cell
 2013-4-19 2013-4-27 2013-5-28

Surgery + Anti-tuberculous medications

2013-9-26 6 months after given
Isoniazid+Rifampin+Ethambutol
• Granuloma formation may not occur in
histological sections, and AFB stains may
be negative.
• Dignosis is difficult. biopsy, culture, PCR
• At times, a clinical diagnosis must be
made and empiric therapy given.
• A combination of anti-tuberculous
medications must be used, especially
when the infection is disseminated.
S7 Erysiploid
• Erysipeloid is an inflammation of the skin caused
by the gram -positive bacillus Erysipelothrix
rhusiopathiae . It occurs most frequently among
those who handle animals , meat or seafood.
• The bacilli typically enter the skin via a minor
trauma in a hand or finger . After I ～ 4 days
incubation, a sharply circumscribed, painful ,
edematous erythema appears. The lesion tends
to enlarge centrifugally, and heal at the center.
• Usually no systemic symptoms. Uncommonly,
associated with bacteremia and aortic valvulitis.
• Penicillin & tetracycline are extremely effective.
Erysipeloid of hand A well-demarcated, violaceous,
cellulitic plaque (without epidermal changes of scale or
vesiculation) on the dorsa of the hand and fingers, occurred
following cleaning fish; the site was somewhat painful,
tender, and warm.
• Erysipeloid often occurs in persons working as
farmers ,butchers , cooks or fishermen , who are
infected by direct contact with infected animals
or contaminated meat . This is a severe bacterial
infection that may involve multiple organs other
than the skin and usually has an incubation
period of 1 to 4 days .
• The prodromal symptoms often present as low
grade fever , headache and malaise with pain at
the infected area . A few days later , the skin
lesions appear on the hands as painful erythema
, which extends and spreads to form a dark red
to purple , well-demarcated , edematous lesion
with slightly elevated edges . The purulent
exudate or ulceration is rarely seen , but tiny
blisters may develop on the surface. Pricking
pain and itching are both reported from
patients .If the lesion involves the finger , it may
be difficult to bend the finger due to pain and
swelling .
Clinical Manifestations - three types
① Localized cutaneous type
② Diffuse cutaneous type
③ Generalized or systemic type
Diagnosis ：
① the clinical features
② history of contact with animals or raw
meat and trauma on the hands
Differential Diagnosis ：
①Erysipelas: cardinal red with significant
edema on leg or face.
②Cellulites: acute courses with apparent
systemic symptoms such as chills , fever
and headache
 Treatment
① Penicillins are the first line of treatment for
any type of erysipeloid .
② Tetracycline ， Ciprofloxacin + rifampin ，
Erythromycin + rifampin for patients allergic
to penicillin.
The End