BACTERIAL SKIN

INFECTION
Dr. H.W. WONG Dip.Derm.
DermatoVenereology Dept.
Medical Faculty UKRIDA

Classification

Pyoderma:
1. acute pyoderma; impetigo etc.
2. chronic pyoderma; hydradenitis
suppurativa etc
3. systemic infection; SSSS etc
4. other bacterial infection; erythrasma etc
Non Pioderma = Mycobacterial infections:
TBC, Leprae, Frambusia
2

Bacterial Skin Infection

- Resident or transient bacteria in the
epidermis
& mucosa.
- Invade the skin weak barrier
function : hair
follicles, sweat glands or sites of minor
trauma.
- Severity of infection relative balance
between the amount & virulence of the
bacteria and the defenses of the host.
- Causative bacteria identified by
culture &
microbial sensitivity test to choose
3
the appropriate antibacterial drugs

Bacterial Skin Infection

4 main subtypes of bacterial infections,
classified
by the clinical features :
Acute cutaneous infections (acute pyoderma)
Chronic cutaneous infections (chronic
pyoderma)
Systemic infections caused by toxins that are
produced by bacteria
Specific clinical features that are caused by
specific bacteria
4

A. Acute pyodermas
1. Impetigo
1) Bullous impetigo
2) Non bullous impetigo
2. Erysipelas
3. Cellulitis
4. Folliculitis
5. Furuncle, Carbuncle
6. Bacterial paronychia
7. Multiple sweat gland
abscesses
in infants
5

B. Chronic Pyoderma
1.
2.

3.

1. Hydradenitis suppurativa
2. Keloidal folliculitis =
Dermatitis papillaris capillitii
3.Pyodermia chronica
glutealis

C. Systemic
Infections

1. Staphylococcal scalded-skin
syndrome (SSSS)
2. Toxic shock syndrome (TSS)
3. Scarlet fever (Streptococcal
infection)
4. Necrotizing fasciitis
5. Gas gangrene
6. Sepsis
7

D. Other bacterial
infection
1.
2.
3.
4.
5.

Trichomycosis palmellina
Erythrasma
Actinomycosis
External dental fistula
Nocardiosis

A. Acute pyodermas

1. Impetigo

Synonym: Impetigo contagiosa

Bacterial infection occurs under the horny cell layer,
producing
toxins that cause blisters and crusts.
The infection spreads by autoinoculation.
Infants are most frequently affected.
Impetigo is divided into :
bullous impetigo, in which blistering is caused by
Staphylococcus aureus
nonbullous impetigo, in which crusts form from groupA b-hemolytic Streptococcus infection.
Antibiotics and keeping skin clean are the main
treatments
10

1) Bullous impetigo

Bullous impetigo occurs most commonly in

infants under age 3, during the summer.
It often spreads through epidemic outbreaks at
daycare centers or nursery schools.
It first occurs at a minor trauma, eczema, or
atopic dermatitis that is scratched and affected.
Bullous impetigo begins as an itching and
slightly inflammatory vesicle that enlarges and
forms flaccid blisters.

11

Bullous impetigo

The blisters easily break and become

erosive, forming new blisters by spreading
peripherally or by being dispersed to distant
locations
Bullous impetigo is transmitted by contact
with an infected person.
Nikolskys sign is negative.
It tends to heal without scarring; however, it
may progress into staphylococcal scaldedskin syndrome
12

Pathogenesis

Staphylococcus aureus proliferate in the

horny cell layer, producing exfoliative toxin
(ET), which leads to intraepidermal blisters.

13

Differential Diagnosis

Insect bites, in which blisters are severely

inflammatory and contain sterile components can
be distinguished from bullous impetigo.
In staphylococcal scalded-skin syndrome, there
are the characteristic features of lesions around
the eyes and mouth, and positive Nikolskys sign;
it should be differentiated from bullous impetigo
Cases whose onset is in adulthood should be
differentiated from pemphigus foliaceus

14

Treatment

The skin should be kept clean.

To prevent transmission, patients should not
share towels until crusts form.

Topical application of antibiotic ointments and

oral cefem antibiotics are useful.

15

2) Nonbullous impetigo
Synonym: Streptococcal impetigo

Clinical features, Epidemiology

A few blisters form.
Nonbullous impetigo begins as small
erythema,followed
by multiple pustules and formation of yellowishbrown
crusts
The crusts are thick and firmly adherent; they
discharge pus when pressured.
Pain and swelling occur in the regional lymph node,
often accompanied by pharyngeal pain and fever.
16

Clinical features, Epidemiology

Unlike in bullous impetigo, the onset of

nonbullous impetigo is acute and is
independent of age and season.
The prevalence has been increasing among
patients with atopic dermatitis.

17

Pathogenesis

It is mainly caused by subcorneal infection of

group-A b hemolytic Streptococcus
(Streptococcus pyogenes).

18

Differential diagnosis

It is difficult to distinguish nonbullous impetigo

from Kaposis varicelliform eruption,
particularly in children with atopic dermatitis.
The two conditions may occur at the same
time.

19

Treatment

Oral antibiotics are the first-line treatment

Urine analysis is conducted in cases with
streptococcal nonbullous impetigo, because
glomerulonephritis may occur as a
complication.
To prevent nephritis, administration of oral
antibiotics is continued 10 days after
remission of the eruptions
20

2. Erysipelas

It is most often caused by group-A b-hemolytic

streptococcal infection (Streptococcus pyogenes).
It occurs with sudden fever.
The face is most frequently affected.
Sharply demarcated edematous erythema rapidly
spreads
Intense tenderness and heat sensation are present.
Because Streptococcus pyogenes is not easily
detected by culture, ASO and ASK values are also
measured.
Penicillin antibiotics are the first-line treatment.
21

Clinical features

Sharply demarcated edematous erythema

accompanied by chills and fever occurs
suddenly, frequently on the face and legs.
The erythema surface is tense and glossy.
There is intense tenderness.
The eruptions spread rapidly and
centrifugally.
Blistering may occur on the edematous
erythema (erysipelas bullosa).
22

Clinical features

When the face is involved, first one side is

affected and soon the other side is affected
Systemic symptoms such as fever, nausea
and vomiting are present.
In about 1 week, the eruptions and fever
disappear.
The eruptions may recur repeatedly on
previously affected sites; this is called
recurrent erysipelas
23

Pathogenesis

Erysipelas is a purulent inflammatory disease that

affects primarily the dermis.
It is most frequently caused by group-A bhemolytic
streptococcus (Streptococcus pyogenes).
Streptococcus pyogenes of other groups (group B in
newborns), Staphylococcus aureus, and
pneumococcus may cause symptoms similar to
those of erysipelas.
The pathogenesis of recurrent erysipelas is thought
to be local lymphatic blockage or inadequate
treatment of erysipelas; the details are unknown.
24

Laboratory findings

Antistreptolysin O (ASO) & antistreptokinase

(ASK) as a result of streptococcal infection.
Elevated erythrocyte sedimentation rate,
leukocytosis (left shift of the nuclei in
leukocytes) and CRP positive are observed
The rate of bacterial detection from tissue
fragment or aspirated tissue fluid is low
Streptococcal bacteria can be detected by
PCR.
25

Differential diagnosis

Cellulitis is more deeply seated than

erysipelas and its erythema edges are less
clearly defined.
Necrotizing fasciitis can be distinguished from
erysipelas by the rapidly progressing necrotic
lesions and intense systemic symptoms.
Insect bites, thrombophlebitis, Sweets
disease, herpes zoster, and carcinoma
erysipelatodes
26

Treatment

Antibiotics such as penicillin drugs and nextgeneration oral cefem are administered.
Treatment is continued for 10 days after
remission to avoid recurrence and to prevent
the complication of nephritis.

27

3. Cellulitis

This acute purulent inflammation occurs

extensively in the deep dermal layer and
subcutaneous tissue
Vaguely demarcated erythema, swelling,
localized heat sensation, and sharp pain
occur suddenly in the face and extremities.
It may progress to necrotizing fasciitis or
septicemia.
The main treatments are bed rest and
parenteral antibiotics.
28

Clinical features

The face and extremities, particularly the lower legs, are

most frequently involved.
Cellulitis begins with ill-demarcated erythema, swelling
and localized heat sensation, quickly becoming intense
infiltration that is accompanied by tenderness and
spontaneous pain
Although the infiltration is usually absorbed in the skin
over time and heals, a pustule may form at the soft
center of the lesion
Systemic symptoms such as fever, headache, chills and
arthralgia are present.
Cellulitis may progress to necrotizing fasciitis or
septicemia.
29

Pathogenesis

Most cases of cellulitis are caused by

Staphylococcus aureus.
Group-A b-hemolytic Streptococcus and Hemophilus
influenzae are among the causative species.
Bacteria usually invade the skin through a minor
trauma, cutaneous ulcer, folliculitis or tinea pedis,
causing cellulitis secondarily; however, the entry
route may not be identifiable.
Localized impairment in venous circulation and
lymphatic edema may induce cellulitis.
30

Laboratory findings

Elevated erythrocyte sedimentation rate,

leukocytosis (left shift of the nuclei in
leukocytes), and CRP positive are observed.
Hepatic enzyme levels increase in some
cases.
Bacteria are easily detected from the pus in
the lesion.
Bacterial culture is more difficult to perform in
cases without pus discharge.
31

Differential diagnosis

Lesions caused by erysipelas are superficial

and the progressive lesions are sharply
circumscribed; however, differentiation from
cellulitis is difficult
Necrotizing fasciitis is accompanied by
purpura, blisters, bloody blisters and severe
systemic symptoms.
Thrombophlebitis, erythema nodosum, insect
bites and herpes zoster
32

Treatment

Systemic administration or intravenous cefem

antibiotics and bed rest are the main
treatments.
Necrotizing fasciitis is suspected when nonlocalized symptoms present, including high
fever, abnormally high leukocyte and CRP
levels, and marked systemic symptoms.

33

4. Folliculitis

Synonym: Acne vulgaris

It is a localized bacterial infection in a single hair
follicle.
It is a pustule accompanied by erythema.
Folliculitis that occurs on the face in puberty is called
acne vulgaris.
It may progress to furuncle or carbuncle.
The main treatments are skin care and topical or oral
antibiotics.
34

Clinical features

Erythema and pustule occur at the hair follicle

The skin lesion forms crust in several days and
heals without scarring in most cases.
Superficial folliculitis that causes multiple eruptions
on the face especially in puberty is called acne
vulgaris
Deep-seated folliculitis is accompanied by intense
inflammatory symptoms and may progress to
furuncle or carbuncle in some cases.
The deep-seated folliculitis in the barba areas is
called sycosis vulgaris
35

Pathogenesis

A hair follicle is infected by Staphylococcus

aureus or Staphylococcus epidermidis.
A minor trauma, obstruction and scratch
around a hair follicle, or topical application of
steroids may induce the infection.
The hair follicle becomes inflamed.

36

Treatment

When there are only a few eruptions,

folliculitis heals spontaneously and can be
left untreated.
Topical or oral antibiotics are used in cases
with multiple eruptions.

37

5. Furuncle, Carbuncle

It is advanced folliculitis.
Pustular plug forms at the center of the skin lesion.
There is purulent swelling.
It is called a furuncle when a single hair follicle is
involved, and a carbuncle when the furuncle
spreads to multiple hair follicles.
When a furuncle occurs over a long period of time or
when multiple furuncles occur at the same time, it is
called furunculosis.
Administration of antibiotics, and incision and
drainage of pus are the main treatments
38

Clinical features

A small red follicular papule or pustule (folliculitis)

appears and is accompanied by induration.
Reddening, tenderness, spontaneous pain, and
localized heat sensation become marked.
The pustule develops a pustular plug.
The induration softens and becomes an abscess.
Inflammatory symptoms quickly subside when the
pus discharges, and in 1 or 2 weeks the furuncle
heals leaving a small scar

39

Clinical features

When a furuncle repeatedly recurs over a long

period of time or when multiple furuncles occur,
it is called furunculosis.
Immunodeficiency from diabetes or malignant
tumor underlies many cases of furunculosis.

40

Clinical features

A carbuncle is a further aggravated furuncle

whose inflammation spreads to multiple
peripheral hair follicles.
It is accompanied by sharp pain, fever and
systemic fatigue
Areas of stretching, such as the back, thighs and
nape of the neck, are often involved.
Carbuncles are dome-shaped, reddening or
swelling induration with several pustular plugs at
the top
41

Pathogenesis

In most cases, Staphylococcus aureus

invades a hair follicle and causes follicular
inflammation
An underlying condition such as diabetes is
present in the most severe cases of furuncle
or carbuncle.

42

Diagnosis

Painful, pointy red swelling occurs in a hair

follicle.
Diagnosis can be confirmed when a pustular
plug is seen in the center of the eruption
It may be difficult to differentiate infectious
epidermal cyst from furuncle or carbuncle.

43

Differential diagnosis

An infectious epidermal cyst is an inflamed

cyst that develops abscesses.
White gruel-like contents and the cyst wall
discharge from the dome-shaped elevation by
small incision.
Hidradenitis suppurativa occurs, most
frequently on sites with apocrine sweat
glands, such as axillary fossae.
It progresses slowly, and pustular plugs do
not form.
44

Treatment

Antibiotics effective against Staphylococcus

aureus are administered orally, or IV in severe
cases.
Incision and drainage of pus is conducted in
cases with palpable pulsation.

45

6. Bacterial paronychia

It is purulent inflammation in the fingers and

toes from paronychia.
The widely used term whitlow often refers to
herpetic whitlow.
The main symptom is pulsating reddening
accompanied by sharp pain.
Bed rest, administration of antibacterial
drugs, and incision and drainage of pus are
the main treatments.
46

Clinical features,
Classification

Intense throbbing pain, swelling, reddening

and heat sensation occur in the periungual
region and distal portion of the finger
The nail plate may appear green when the
infection is caused by Pseudomonas
aeruginosa, which produces that pigment.
The nail may exfoliate.

47

Pathogenesis

The main causes of bacterial paronychia are

Staphylococcus aureus, Staphylococcus
pyogenes, coliform bacilli, and Pseudomonas
aeruginosa.
Minor trauma and ingrown nails often induce
it.

48

Treatment

Cooling the affected site and administering

antibiotics that are effective against
Staphylococcus aureus and Staphylococcus
pyogenes are the main treatments.
Incision and drainage of pus are necessary in
many cases.

49

Differential diagnosis

Mucous cyst, glomus tumor, metastatic

cancer, Oslers node, herpes whitlow and
candidal paronychia should be differentiated
from whitlow.

50

7. Multiple sweat gland abscesses

in infants
Multiple
painful pustules and subcutaneous
induration occuron the face, scalp and
buttocks of newborns and infants, most
frequently in summer.
The eruptions mix with miliaria.
Miliaria appears first as a precursor in which
Staphylococcus aureus infection occurs,
resulting in multiple sweat gland abscesses.
51

7. Multiple sweat gland abscesses

in infants

Eccrine sweat glands are mainly involved.

Antibacterials against Streptococcus are
administered.
The skin should be kept clean for preventive
purposes by frequent changing of clothes

52

B. Chronic pyodermas

53

Chronic pyodermas

Chronic pyoderma is a general term for chronic

purulent diseases in which multiple obliterative
lesions of hair follicles are infected by bacteria,
leading to prolonged inflammatory reaction or
granulomatous inflammation.
Many diagnostic names for chronic pyoderma exist;
in fact, they all refer to the same disease.
The axillary fossae, scalp and buttocks are most
commonly involved.
Squamous cell carcinoma may originate from these
conditions.
54

1. Hidradenitis suppurativa

This is hidradenitis in the opening of a hair

follicle that is contained in the apocrine sweat
gland.
The follicular opening is blocked by a keratin
plug, leading to secretion deposition where
Staphylococcus aureus infects
One or several subcutaneous nodules about 5
mm in diameter occur, most frequently on the
axillary fossae of women.
55

Hidradenitis suppurativa

The nodules soften, rupture,excrete pus, and

heal with scarring.
Hidradenitis suppurativa often becomes chronic.
Other sites with apocrine sweat glands,such as
the genitalia, anus and breasts, may also be
involved.
Administration of antibiotics and incision and
drainage of pus are the main treatments

56

2. Dermatitis papillaris capillitii

This is also known as keloidal folliculitis.

Folliculitis appears multiply and continuously on the
occipital and nuchal region of middle-aged men.
Infiltration of the lesion gradually becomes intense,
and connective tissue proliferates and forms a
keloidal plaque.
Abscess formation and secretion of pus may be
present in severe cases.
Administration of antibacterials is thefirst-line
treatment. Plastic surgery may be necessary.

57

3. Pyodermia chronica glutealis

Middle-aged men are most frequently affected.

Acne-like pustules or papules appear on the lumbar
region, genitalia, and thighs, gradually coalescing
into a large infiltrative plaque.
Abscesses with intricately netted fistulae form, and
these excrete pus when pressed
There is hidradenitis suppurativa or acne conglobata
as an underlying disease in many cases.
Systemic administration of antibiotics, incision a and
drainage of pus,and removal and skin graft are the
main treatments.
58

C. Systemic infections

59

1. Staphylococcal scalded-skin
syndrome (SSSS)
Synonym: Staphylococcal toxic epidermal
necrolysis (S-TEN)

It is caused by exfoliative toxins of Staphylococcus

aureus in the epidermis.
It occurs most frequently in infants and children up to
age 6.
A fever and reddening around the mouth or eyes first
appear, followed by painful exfoliation, erosion and
blistering.
Nikolskys sign is positive.
Systemic management and care, and administration
of antibiotics are the main treatments.
60

Clinical features

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 reddening and blistering around
themouth, nostrils, and periocular area.
This is accompanied by systemic symptoms, such
as a fever of about 38C, irritability, and poor
appetite.
Wrinkles and fissures around the mouth, eye
discharge and crust formation result in
characteristic facial features.
61

Clinical features

Erythema occurs on the neck, axillary fossae, and

groin, and the whole body skin begins to exfoliate as if
burned, which leads to erosion
Skin at normal sites also exfoliates easily by friction
(Nikolskys sign is positive).
Sharp pain is present.
The mucous membranes tend not to be affected.
Exfoliation in the scalp can occur in rare cases.
SSSS begins to heal after exfoliation is accelerated
by systemic administration of antibiotics.
The entire course of SSSS is 1 to 2 weeks
62

Pathogenesis

SSSS is caused by exfoliative toxin (ET)

produced by Staphylococcus aureus.
The nasopharynx, conjunctivae, external
ears,and navel are most frequently infected.
When ET spreads to the whole body by blood
circulation, desmoglein 1, a desmosome
structural protein, is broken.
Pemphigus foliaceus-like acantholytic and
intraepidermal blisters form on the upper
epidermal layer.
63

Pathology

Acantholysis, lacunae and infiltration of

polymorphonuclear cells are observed under
the horny cell layer and in the granular cell
layer.

64

Diagnosis

SSSS can be diagnosed by the characteristic

facial features, burn-like systemic epidermal
exfoliation, marked Nikolskys sign, and
normality of oral mucosa

65

Differential diagnosis

Most cases of toxic epidermal necrolysis

(TEN) are induced by drugs.
Histopathologically, there is necrosis in all
epidermal layers and severe infiltration to the
mucous membranes.
Infants are rarely affected by TEN.
In widely spread multiple bullous impetigo,
the characteristic facial features of SSSS do
not occur and Nikolskys sign is negative.
66

Treatment

Hospitalization and systemic care including

transfusion and intravenous antibiotics that are
effective against Staphylococcus aureus are given.
The affected site is sterilized and treated with topical
application of ointments that contain antibiotics or
petrolatum.
SSSS tends to have a good prognosis; however, it
may become severe, with sepsis or pneumonia
appearing as complications in infants and in adults
with immunodeficiency

67

2.Toxic shock syndrome (TSS)

Synonym: Staphylococcal toxic shock syndrome

(STSS)

TSS is caused by an exotoxin called toxic shock

syndrome toxin (TSS toxin-1 or TSST-1), which is
produced by infection and proliferation of
Staphylococcus aureus.
It may occur in burn patients and women who use
sanitary tampons.
TSS is a systemic toxic disease whose main
symptoms are acute fever, decreased blood
pressure, scarlet-fever-like erythema, and multiple
organ dysfunction

68

Toxic shock syndrome (TSS)

Diffuse erythema, chills, headache, and

arthralgia on the whole body are present,
leading to systemic fatigue, vomiting and
diarrhea.
Antibiotics, mainly b-lactum drugs, are useful
in large doses, in combination with
immunoglobulin preparations.

69

3. Scarlet fever (Streptococcal

infection)

It is erythematous exanthema and enanthema

caused by group-A b-hemolytic streptococci (GAS).
It begins with pharyngeal pain and high fever.
It is characterized by reddening of the tongue
(strawberry tongue) and dense erythema on the
whole body.
Eruptions do not appear around the mouth (perioral
pallor).
Increased antistreptolysin O has diagnostic value.
Penicillin is administered.
70

Clinical features

Scarlet fever most frequently occurs in late childhood.

The incubation period is known to be 2 to 3 days.
It begins with a sudden fever and pharyngeal pain,
soon followed by strawberry tongue.
At the early stages, tongue fur which is often referred
to as white strawberry tongue is seen in many
cases.
However,the tongue fur resolves in a day or two,
leaving the typical strawberry tongue.

71

Clinical features

Eruptions appear 1 to 2 days after onset of

streptococcal infection.
Patchy, vivid red papules appear on the neck, axillary
fossae, and medial thighs, spreading over the whole
body.
The eruptions may be accompanied by itching and
burning.
Diffuse erythema appears on the face, except at the
peripheries of the mouth and nasal alae (perioral
pallor).
Hemorrhagic lesions and systemic lymph node
enlargement also occur
72

Clinical features

As the fever subsides on the third or fourth

day after onset, the eruptions begin to
disappear.
After exfoliation, the eruptions heal without
post inflammatory pigmentation.

73

Pathogenesis

Eruptions are caused on the whole body by

an exotoxin produced by Streptococcus
pyogenes.
This bacterium first infects the palatal tonsil
or skin.

74

Complications

Post-infectious complications of
Streptococcus pyogenes may occur, such as
acute glomerulonephritis and rheumatic
fever.

75

Laboratory findings

Elevated levels of ASO and ASK,

leukocytosis, and left shift of the nuclei in
leukocytes are caused by streptococcal
infection.
Bacteria are detected from the primary
infection site, such as the pharynx.
The rapid diagnostic test kit is also useful,
although the detection sensitivity is relatively
low.
76

Differential diagnosis

Rubella, Kawasaki disease and drug eruptions

should be differentiated from streptococcal
fever

77

Treatment, Prognosis

Oral penicillin G is the first-line treatment.

Although eruptions disappear in 2 to 3 days,
administration of penicillin G should be continued for
at least 2 weeks because if the medication is
stopped early, Streptococcus may proliferate again
in the pharynx, causing complications such as
nephritis or rheumatic fever.
After termination of medication, periodic
examinations such as urine test are necessary to
detect bacteria.

78

4. Necrotizing fasciitis

It is an acute bacterial infection in subcutaneous

tissue and superficial fascia
The extremities and genitalia of persons middleaged and older are most frequently affected.
The main systemic symptoms are reddening and
swelling of skin, ulceration, and fever accompanied
by intense pain.
High doses of antibiotics at the early stages and
surgical dbridement are the main treatments.
Multiple organ failure may lead to death.
79

Clinical features

The extremities (lower legs in particular), genitalia and

abdomen of persons over age 40 are most frequently
affected.
Necrotizing fasciitis begins with localized reddening and
swelling that rapidly progress with marked systemic
symptoms.
In 1 to 3 days, purpura, blisters, bloody blisters, concave
necrosis and ulceration occur
The sensation of touch is reduced according to the
progression of the fasciitis.
Even when the periphery of the lesion appears normal to
the naked eye, the subcutaneous tissue is affected

80

Clinical features

Necrotizing fasciitis is characterized by

intense systemic symptoms such as high
fever, severe arthralgia, muscle pain, shock
and multiple organ failure.
Necrotizing fasciitis of the genitalia is called
Fourniers gangrene.
Necrotizing fasciitis frequently occurs as a
complication of toxicshock-like syndrome
(MEMO).
81

Pathogenesis

The main causative bacteria are Streptococcus

pyogenes and anaerobes such as Bacterioides
fragilis and Peptostreptococcus anaerobius.
Streptococcus pyogenes may infect healthy
persons, leading to a sudden onset of necrotizing
fasciitis.
Anaerobic bacteria tend to infect individuals with an
underlying disease, such as diabetes.
In some cases, a micro-injury or tinea pedis induces
necrotizing fasciitis; however, details of the
pathogenesis are unknown.

82

Pathology

Edema is marked throughout the dermis.

Panniculitis, necrosis, blockage of the blood
vessels, and infiltration of polymorphonuclear
leukocytes occur from the lower dermal layer
to the underlying fat tissue and fascia

83

Laboratory findings

Leukocytosis, left shift of the nuclei in

leukocytes, elevated levels of CRP, liver
failure and coagulation abnormality (when
DIC is caused) are present.
Prior to administration of antibiotics, bacteria
are detected from the puncture fluid,
necrotizing tissue at dbridement, and blood.
MRI, CT, and X-ray images are helpful in
testing for the depth and size of lesion and for
any retention of gas.
84

Diagnosis

Prompt diagnosis and initiation of treatment

are important.
Necrotizing fasciitis is diagnosed by its
sudden onset, rapid progression, intense
systemic symptoms, purpura, blisters, bloody
blisters and the depth of necrosis measured
by dbridement.
Bacterial culture and skin biopsy are
conducted for differential diagnosis.
85

Differential diagnosis

Some cases are difficult to differentiate from

ordinary cellulitis; however, necrotizing fasciitis is
characterized by rapid progression of skin lesion,
purpura and bloody blisters, and intense systemic
symptoms.
The spread of inflammation and involvement of
fascia can be determined by MRI.
Gas gangrene is found in the muscle layer of the
lesion.
Marked retention of gas is observed by X-ray.
The causative bacteria are Clostridium.

86

Treatment, Prognosis

Large doses of antibiotics that are effective

against the pathogen (e.g., drugs containing
penicillin, clindamycin) and surgical
dbridement in the early stages are essential.
Unless treated in the early stages, the
prognosis is extremely poor.

87

5. Gas gangrene

Most cases are caused by anaerobic bacteria

such as those of the genus Clostridium.
Mortality is high.
Intense systemic symptoms, muscular
necrosis and aerogenesis occur. There is
crepitation from gas in the tissues.
Rapid incision and lavage of the lesion, large
doses of antibiotics, and hyperbaric oxygen
therapy are the main treatments.
88

Clinical features

Six to 72 hours after injury, gas gangrene

begins with a localized sharp pain.
Systemic symptoms such as chills and
tachycardia occur.
The skin becomes dark purple or blackish.
Hematoid serous blisters form.
Liquefactive necrosis occurs in muscle
tissue.
89

Clinical features

The lesion swells with the gas.

The affected site releases foul odor.
When the site is pressed, the gas moves,
causing crepitation.
Bubbles are observed by X-ray. If left
untreated, exotoxin circulates through the
bloodstream to the entire body, leading to
jaundice, DIC or shock, and resulting in
death.
90

Pathogenesis

Gas gangrene is most frequently caused by

Clostridium perfringens (formerly Clostridium
welchii), Clostridium oedematicus, Clostridium
septicum and Clostridium histolyticum, but in some
cases by non-Clostridium bacteria.
The causal bacteria exist in soil and sometimes in
the feces of humans and animals, invading the body
through a severely crushed and contaminated
wound.
These bacteria grow in the anaerobic environment
and produce an exotoxin containing proteolytic
enzymes, which induce hemolysis and shock.
91

Treatment, Prognosis

Quick incision, lavage and surgical dbridement are

important.
At the same time, penicillin G or cefem antibiotics
are administrated in large doses.
Proliferation of anaerobic bacteria can be prevented
by opening the lesion.
When the bacteria are anaerobic,hyperbaric oxygen
therapy is useful.
Systemic care is performed for shock, kidney failure
and DIC.
Amputation of extremities may be necessary in
severe cases.
92

6. Sepsis

Sepsis occurs when a localized cutaneous

infection such as in abscess, cellulitis or
erysipelas aggravates and disseminates in
the blood flow.
The bacteria themselves or thrombosis
caused by bacteria in the blood induces
septic vasculitis, resulting in septicemide
formation including erythema, purpura,
bloody blisters and pustules.
93

7. Oslers node

This is transient, painful, nodular erythema that often

accompanies subacute bacterial endocarditis.
Elevated erythema of 5 mm in diameter occurs on
the finger pads, thenar and hypothenar eminences.
Sharp pain occurs as a precursor, and a brown patch
appears and disappears in 1 or 2 days.
Oslers node accompanied by painless erythema or
infiltrative purpura is called Janeway lesion.
Allergic reaction against the bacteria and vascular
blockage are thought to be the causes in all cases.
Oslers node is known to appear in 15% of infectious
endocarditis cases.
94

D. Other bacterial
infections

95

1.Trichomycosis palmellina

It occurs most frequently in young patients with

hyperhidrosis and poor hygiene.
Bacteria in colloidal suspension, ranging from
yellowish brown to white, attach in clusters to
axillary or pubic hairs.
The hairs appear to be yellowish and swollen.
The condition may be accompanied by foul odor.
The pathogenesis in most cases is infection caused
by Corynebacterium tenuis, which fluoresces as
yellow, white, or blue under Woods lamp.
The treatments are hygiene improvement,
antisepsis, shaving of hair, and topical tetracycline
96

2. Erythrasma
Clinical features:

Moist intertriginous regions such as the genitocrural

region, axillary fossae and interdigital clefts are most
commonly involved.
Erythrasma presents as sharply margined, red or
reddish- brown patches on whose surface thin and
fine scales attach.
Papules or blisters do not occur.
The center of the lesion does not heal, whereby
erythrasma can be distinguished from tinea.
Erythrasma tends to be asymptomatic, and there
may be itching and burning in rare cases.
97

Pathogenesis

Erythrasma is caused by infection in the

horny cell layer by Corynebacteria called
diphteroids.
It often occurs in patients with diabetes,
obesity or hyperhidrosis.
It is thought to be an opportunistic infection

98

Diagnosis, Examination

It is difficult to differentiate erythrasma in the

toe clefts from tinea pedis; however, coral-red
fluorescence of erythrasma observed under
Woods lamp is diagnostic.
Since erythrasma and tinea pedis are present
together in many cases, mycological
examination of scales is necessary.
Gram-positive short bacilli are observed in
the scales of the lesion.
99

Treatment

Topical imidazole antifungal agents and oral

erythromycin are effective.

100

3. Actinomycosis
Clinical features, Classification

Actinomycosis is classified by the primary site

into cervicofacial actinomycosis, thoracic
actinomycosis and abdominal actinomycosis.
Of these three subtypes, cervicofacial
actinomycosis,which is often induced by dental
caries and accompanied by skin lesions,
accounts for about half of all actinomycosis
cases.
101

Clinical features,
Classifica

Thoracic actinomycosis and abdominal

actinomycosis are accompanied by a lesion
in the internal organs; unless there is a fistula
that affects the skin, these two subtypes are
not addressed in dermatology
Reddening, swelling and induration occur,
forming a dark red subcutaneous nodule

102

Clinical features,
Classifica

The nodule partly softens and forms an

abscess, leading to a fistula from which pus
excretes for a long period of time.
A chronic suppurative granulomatous lesion
is produced.
Mild fever and pain are present in most
cases.
Actinomycosis is nearly asymptomatic;
however, there is difficulty opening the mouth
when the masticatory muscle is involved.
103

Pathogenesis

Actinomyces israelii, a microbe resident in

the human oral cavity, tonsillar fossae and
dental plaques, invades the body from a
minor injury, proliferates and forms a lesion.
Once believed to be a fungus, Actinomyces
israelii has been found to be a bacterium.

104

Pathology

Microabscess forms in parts of fibrotic

inflammatory granulomatous tissue.
Actinomycosis is characterized by bacterial
mass in the microabscess called sulfur
granule

105

Differential diagnosis

Nocardia infection causes lesions similar to

those of actinomycosis.
External dental fistula and inflammatory
epidermal cyst should be differentiated from
actinomycosis.

106

Treatment
Penicillin, tetracycline and cefem antibiotics
are administered orally.

107

4. External dental fistula

As a result of progression of dental caries or

alveolar osteitis, a fistula forms from which
pus is excreted
Dental treatment is necessary. It may be
misdiagnosed as subcutaneous ulcers such
as epidermal cyst or actinomycosis.

108

5. Nocardiosis
Clinical features
Skin lesions caused by nocardiosis are
divided by morphology into three subtypes:
nocardia mycetoma, which progresses in a
process very similar to that of actinomycosis;
localized cutaneous nocardiosis, in which
subcutaneous abscess forms; and cutaneous
lymphatic nocardiosis, in which the lesion
enlarges on skin over the lymph vessels.
This section focuses on nocardia mycetoma
109

Clinical features

The legs are most frequently involved.

Dark red subcutaneous nodules appear after
multiple reddening, swelling and induration.
The nodules form abscesses where fistulae are
produced, excreting pus for a long period of time.
Some of the pus may be granular.
Opportunistic infectious nocardiosis invades the
lung and progresses in a course similar to that of
bacterial pneumonia.
A skin lesion and a cerebral abscess occur in cases
with hematogeneous dissemination.
110

Pathogenesis

Nocardiosis is infection by the anaerobic

bacteria of the genus Nocardia.
In developing countries, Nocardia in the soil
causes skin lesions.
The bacteria may invade the lung and cause
an opportunistic infection and systemic
nocardiosis.
Nocardia asteroids is the causative species
in most cases.
111

Laboratory findings,
Diagnosis

Pus or sputum smears are examined after

Gram staining.
Cultures are obtained on Sabouraud glucose
medium.
Or Nocardia are identified by skin biopsy.
Infiltration of Nocardia into bone is
investigated by bone X-ray.
Drugs for treatment are chosen by measuring
MIC.
112

Treatment

The most effective drug for each case is

chosen from among sulfate drugs,
minocycline, or penicillin.
The treatment is continued for several
months.
For cases in which all drugs are ineffective or
bone is involved, surgical removal is
performed.

113

Non Pioderma = Mycobacterial inf.

A. Mycobacterial TBC infs

B. Non-tuberculous mycobacterial infs
C. Mycobacterium leprae inf

114

Mycobacterium TBC inf Klasifikasi menurut Pillsbury

1. TBC kutis sejati, bila kuman ada pada
kelainan kulit tsb
2. TBC yang mengikuti vaksinasi BCG
3. Tuberkulid, merupakan id reaction, dimana
kuman tak ditemukan di tempat kelainan, jadi
kelainan kulit disebabkan reaksi alergi, ex:
Bentuk Papul:tuberkulid papulonekrotika,
liken skrofulosorum. Bentuk granuloma:
eritema nodosum , e.induratum
115

TBC kutis sejati

1. Primer
2. Sekunder

A. Skrofuloderma
B. TBC kutis verukosa
C. TBC kutis gumosa
D. TBC kutis orificialis
E. Lupus vulgaris

116

Epidemiologi

1. Lebih banyak pada anak daripada dewasa

2. Perempuan lebih banyak dari laki laki
3. yang paling sering, Skrofuloderma, >80%,
dan TBC kutis verukosa >10%

117

Etiologi

1. Mycobacterium TBC, >90%

2. Mycobacterial atipikal, yaitu M.
scrofulaceum, M rapid grower

118

Patogenesis

1. Penjalaran langsung ke kulit dari organ

bawah kulit yang terkena TBC, Skrofuloderma
2. Inokulasi lgs pada kulit sekitar orifisium
3. Hematogen, TBC kutis miliaris
4. Limfogen, Lupus vulgaris
5. dari selaput lendir yang terkena TBC ex.LV
6. Langsung masuk kulit yg terluka, TBC kutis
verukosa
119

Susunan Kelenjar Getah Bening

Skrofuloderma, sering terjadi, untuk itu perlu

mengerti aliran KGB
1. Sekitar bawah dagu, leher, ex: KGB
submentalis, KGB submandibularis
2. Lipat paha, KGB femoralis
3. Lipat ketiak, KGB axilaris

120

Gambaran Klinik

Afek primer dapat berbentuk papul, pustul

dan ulkus indolen, berdinding gaung dan livid
Masa tunas, 2-3 minggu
Limfangitis dan limfadenitis minggu sd
bulan an
Reaksi tuberkulin menjadi positif disebut
kompleks primer

121

Skrofuloderma

Pembesaran dan pembendungan aliran limfe

didaerah leher, aksila dan inguinal
Biasa berdekatan dengan proses TBC
dibawahnya, TBC tulang, tbc sendi, tbc
kelenjar
Patogenesis : penyebaran per kontinuitatum
dari alat dibawah kulit yang terkena tbc

122

Skrofuloderma, gambaran klinik

Pembesaran KGB, tanpa tanda radang jadi

hanya tumor, limfadenitis tuberkulosa
Konsistensi kenyal, lalu melunak/supurasi
lalu memecah jadi fistel
Muara fistel akan meluas dan berupa ulkus
khas, memanjang , tidak teratur , dinding
bergaung, livid, jaringan granulasi tertutup
pus / krusta, sikatriks dapat terbentuk skin
bridge, dimana sonde bisa masuk
123

Pemeriksaan Lab

1. Lekositosis dan LED meningkat

2. Mantoux test positif
3. Pemeriksaan bakteriologik
4. PA
5. PCR, polymerase chain reaction

124

Pengobatan

Sama dengan TBC paru

1. teratur dan tidak terputus
2. Kombinasi

125

Kriteria penyembuhan

1. Fistel dan ulkus menutup

2. KGB mengecil <1cm, mengeras
3. sikatriks tidak eritematous lagi

126

Non-tuberculous mycobacterial
inf, = Mycobacterial atypical

1. Mycobacterium marinum infection

2. Mycobacterium avium intracellular
complex
3. Mycobacterium fortuitum infrction,
Mycobacterium chelonae infection
4. Mycobacterium kansasii infection

127

Mycobacterium marinum infection

Synonyms= Fish tank granuloma, swimming

pool granuloma
Paling sering terjadi, > 60%
Banyak pada pekerja kolam ikan
Awal karena luka kecil
Onset 2 minggu
Prognosis baik
Tetrasiklin , Rifampisin, untuk 2-3 bulan
128

Mycobacterium leprae infection

Leprosy

129

Leprosy = Kusta

Mycobacterium leprae
Kronik Progresif
Primer menyerang syaraf tepi, kemudian
bermanifestasi di kulit
Dapat menyerang mukosa dan saluran nafas
bagian atas, kelenjar limfe kecuali SSP
Sinonim: Lepra, Morbus Hansen

130

Epidemiologi

Kontak langsung lama erat

Masa tunas sangat bervariasi mean: 3-5 thn
Patogenesis kuman, cara penularan,
sosioekonomi, genetik, reservoir diluar
manusia
Belum ditemukan media artifisial
Bukan penyakit keturunan
Ulserasi, mutilasi, deformitas
131

Etiologi

Mycobacterium leprae
Ditemukan G A Hansen (Norwegia)
Belum dapat dibiak pada media artifisial
Berbentuk basil 3-8 Um x 0.5 Um
Tahan asam, alkohol
Gram positif

132

Gambaran Klinik

1. Anestesi
2. Anhidrosis
3. Alopesia
4. Atrofi
5. Akromi

133

Spektrum
Berdasarkan gambaran klinik dini dan
imunologik, spektrum terbagi :
1. Tipe poler Tuberkuloid TT, stabil
2. Tipe poler Lepromatosa LL, stabil
Diantaranya disebut tipe campuran, Labil
BT borderline tuberkuloid
BB mid borderline
BL borderline lepromatosa

134

Tuberkuloid

Jumlah Makula, satu sampai beberapa

Distribusi : asimetrik
Batas: Jelas
Permukaan, agak kasar
Anestesi, lebih Jelas
Kontraktur, timbul cepat, 1 tahunan

135

Lepromatosa

Makula lebih banyak

Distribusi, simetrik, bilateral menyeluruh
Batas kurang jelas
Permukaan lebih halus
Anestesi kurang jelas
Kontraktur, agak lambat terjadi, bisa 5
tahunan

136

DD/

1.TBC
2. Sipilis
3. Mikosis superfisialis
4. Mikosis fungoidalis
5. Penyakit metabolik endokrin yang
mempengaruhi saraf, DM

137

Pengobatan

DDS
Rifampisin
Clofasimin
Kuinolon
Nsaid jika nyeri sekali

Untuk 6-24 bulan

138