Bacterial Skin

Infections& ACNE
PROF.Dr.Furquana Niaz
MBBS,FCPS(SKIN),
D-DERM(UK),CHPE(DIMC),
AAAMS(DUBAI)
HOD DERMATOLOGY DEPARTMENT
NAIMAT BEGUM HOSPITAL/HAMDARD
MEDICAL UNIVERSITY
 Bacterial
Infection of Skin
The Skin
Definition

Skin is largest organ of body. Maintains

homeostasis, protects underlying tissues and
organs, protects body from mechanical injury,
damaging substances, and ultraviolet rays of
sun.
 Recurrent skin
infections
 Recurrent skin infections should raise
suspicion of colonization
 Staphylococcal nasal carriage
 Poorly controlled diabetes
 Other reasons for immunocompromise (eg, HIV,
 hepatitis,
 advanced age,
 congenital susceptibility).
 S. aureus produces
skin infection
I. Direct infection of skin and adjacent tissues
a. Impetigo
b. Ecthyma
c. Folliculitis
d. Furunculosis
e. Carbuncle
f. Sycosis barbae
II. Cutaneous disease due to effect of bacterial
toxin
a. Staphylococcal scalded skin syndrome
b. Toxic shock syndrome
 ß-hemolytic
streptococcus produces
skin infection
I. Direct infection of skin or subcutaneous
a. Impetigo (non bullous)
b. Ecthyma
c. Erysipelas
d. Cellulitis
e. Necrotizing fascitis

II. Secondary infection

Eczema infection
 Impetigo and
Ecthyma
 Impetigo is a superficial skin infection
with crusting or bullae caused by
streptococci, staphylococci, or both.
 Ecthyma is an ulcerative form of
impetigo.
 Impetigo (Non-Bullous
Impetigo contigiosum
Non-bullous impetigo is a
superficial skin infection that
manifests as clusters of
vesicles or pustules that
rupture and develop a honey-
colored crust.
Impetigo (Bullous) impetigo
circinata)
Bullous impetigo is a superficial
skin infection that manifests as
clusters of vesicles or pustules that
enlarge rapidly to form bullae. The
bullae burst and expose larger
bases, which become covered with
honey-colored varnish or crust.
 Impetigo
Contagiosa


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 Impetigo
Contagiosa

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 Impetigo
Contagiosa


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 Bullous Impetigo

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 Bullous Impetigo

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 Bullous Impetigo


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Ecthyma is a skin infection
similar to impetigo, but more
deeply invasive. Usually caused
by a streptococcus infection,
ecthyma goes through the outer
layer (epidermis) to the deeper
layer (dermis) of skin, possibly
causing scars.
Ecthyma gangrenosum is a
bacterial skin infection (caused
by Pseudomonas aeruginosa)
that usually occurs in people
with a compromised immune
system.
 Ecthyma


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 Folliculitis
 Folliculitis is a bacterial infection of hair
follicles.
 Folliculitis is usually caused by
Staphylococcus aureus but occasionally
Pseudomonas aeruginosa (hot-tub
folliculitis) or other organisms. Hot-tub
folliculitis occurs because of inadequate
treatment of water with chlorine or
bromine.
18
Folliculitis manifests as superficial pustules or
inflammatory nodules surrounding hair follicles.
 Treatment of
Folliculitis
 Cleansing with soap and water.
 Bactroban (Mupirocin).

 Antibiotics: cephalosporin, penicillin

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 Furuncles and
Carbuncles
 Furuncles are skin abscesses caused by
staphylococcal infection, which involve a
hair follicle and surrounding tissue.
 Carbuncles are clusters of furuncles
connected subcutaneously, causing
deeper suppuration and scarring. They
are smaller and more superficial than
subcutaneous abscesses
Furuncles (boils) are tender nodules or pustules caused
by staphylococcal infection. Carbuncles are clusters of
furuncles that are subcutaneously connected.
Carbuncles
 Cellulitis
 Cellulitis
is acute bacterial infection of
the skin and subcutaneous tissue most
often caused by streptococci or
staphylococci.
 Treatment of
cellulitis
 Treatment is with antibiotics. For most patients, empiric
treatment effective against both group A streptococci and S.
aureus is used.

 Penicillin
 cephalexin
 Levofloxacin
 moxifloxacin

 For more serious infections, oxacillin or nafcillin 1 g is given IV q

6 h.

 Immobilization and elevation of the affected area

 Cutaneous Abscess
A cutaneous abscess is a localized
collection of pus in the skin and may
occur on any skin surface.
 Erysipelas
 Erysipelas is a type of superficial cellulitis with dermal
lymphatic involvement.
 Erysipelas is characterized clinically by shiny, raised,
indurated, and tender plaque-like lesions with distinct
margins.
 Erysipelas is most often caused by group A (or rarely
group C or G) β-hemolytic streptococci and occurs
most frequently on the legs and face.
 Other causes - Staphylococcus aureus (including
methicillin-resistant S. aureus [MRSA]),
 Klebsiella pneumoniae,
 Haemophilus influenzae,
 Escherichia coli.
It is commonly accompanied by
high fever,
chills,
malaise.
Erysipelas may be recurrent and
may result in chronic
lymphedema.
Erysipelas is characterized by shiny, raised, indurated,
and tender plaque-like lesions with distinct margins. It is
most often caused by β-hemolytic streptococci and
occurs most frequently on the legs and face.
 Erysipelas

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 Erythrasma
 Erythrasma is an intertriginous infection
with Corynebacterium minutissimum.
 Most common among patients with
diabetes and among people living in the
tropics.
 Staphylococcal Scalded
Skin Syndrome(SSSS).
 Presentation: Febrile, rapidly evolving generalized
desquamation of the skin seen primarily in neonates and
children.
 Begins with skin tenderness and erythema of neck groin, axillae
with sparing of palm and soles
 Blistering occurs just beneath granular layer.
 Positive Nikolsky’s sign

 Etiology: Exotoxin from S. Aureus infection located at a

mucosal surface..
 Differentiate from TENS
 Treatment as before.
 Prognosis is good.

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 Staphylococcal Scalded
Skin Syndrome


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 Staphylococcal
Scalded Skin
Syndrome

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 Scarlet Fever
 Presentation: 24 –48 hrs after Strep. Pharyngitis onset.
 Cutaneous:

 Widespread erythema with 1-2 mm papules. Begins

on neck and spreads to trunk then extremities.

 Pastia’s lines – accentuation over skin folds with

petechia.
 Circumoral pallor

 Desquamation of palms and soles at appox two

wks.
 May be only evidence of disease.
 Other: strawberry tongue

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 Causes: erythrogenic exotoxin of group A Strep.
 Culture to recover organism or use streptolysin O titer
if testing is late.
 TX: PCN, E-mycin, Cloxacillin.

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 Scarlet Fever

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 Scarlet Fever

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 Scarlet Fever

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 Bacterial Infection
of Skin
Lab. Diagnosis

Specimen collection.
1. Skin biopsy
2. Skin swab
3. Pus swab
4. Nasal / skin swab
 Recurrent staphylococcal
infection
 Persistent nasal carriage
 Abnormal neutrophilic chemotaxis
 Deficient intracellular killing
 Immunodeficient status
 D.M.
ACNE
 Definition:

Is a chronic inflammatory disorder of the

pilosebaceous apparatus of certain body area
(Face , Shoulder & upper back) ch by
polymorphic skin eruption.
 Incidence:

Acne affects all skin types, the male and female

ratio is virtually the same but tends to be more
severe in males.

85% affects the age group 12 – 24 years

8% affects the age group 25 – 34 years
3% affects the age group 35 – 44 years
 Etiology:
1. Genetic Aspect, (Acne runs in family)
2. other example: XXY syndrome.
3. Occupation (Environmental, Mechanical) e.g.
exposure to acnegenic mineral oil (Pomade
acne),
4. Drugs Oral and topical Hydrocortison
5. (Steroid acne), Lithium, Hydantoin,
contraceptives
6. Endocrine Factors (Recalcitrant Acne, PCO
MARSH Syndrome) .
 Pathogenesis: ( three main
steps recognized and
hypothesized)
1. Follicular Hyperkeratosis (the cause not fully
understood)
Fig 1 Fig 2

Fig 3
Perifollicular
Hyperkeratosis
histology
 Seborrhoea is a common feature between
patients with acne.

2. Abnormal production of abnormal sebum

3. Colonization of the affected unit with
bacteria Propionibacterium acne

Fig 5

Propionibacterium
acne
 P acne is a potent activator of complement via
classical pathway
Fig 6 Fig 7
Propionobacterium acne lipases act on sebaceous fatty
acid (Triglycrides) to release irritant free fatty acid and
low-molecular- weight peptide an extra cellular factor
that penetrate the follicular wall and stimulate
Polymorphs and Lymphocytes initiating inflammation

Fig 8
Blockage of duct
 Clinical features: (Acne and
acne related Disorders)

1. Acne Vulgaris:
Papules: (Less than 0.5 cm)
 Comedones (Open “Blackheads” or closed
“Whiteheads”)
 Open Comedones (Blackheads)

Fig 10 Fig 11

Open
Comedones
 Closed Comedones (Whitehead)

Fig 12 Fig 13

Closed
Comedones
  Inflammatory papules

Fig 14 Fig 15

Inflammatory
papules
  Pustules :

Fig 16 Fig 17

Pustules
  Nodule (more than 0.5 cm)

Fig 18 Fig 19

Nodule
  Cystic acne: the cysts are usually large 1-
4cm
Fig 20 Fig 21
Fig 22
3. Neonatal Acne and Infantile Acne

 Neonatal acne
 : cause unknown but some believed is due to
passing of Transplacental androgen other
suggest the role of Mlalassezia furfur and
sympodalis . affect 1 in 5 mainly inflammatory
comedones on nose and cheeks affect new born
between the 1st and 6th week of age
Fig 23
 Infantile Acne:
 affect males more than females, usually
between 3 and 6 months of age, and tend to
be severer than the neonatal one and
believed to be due to Endogenic androgen
from the infant’s gonads.
Fig 24
 4. Recalcitrant Acne

Affect Women and associated with (Adrenal

hyperplasia "11-B- or 21-B hydroxlase
deficiencies) acne is usually nodulocystic
 5. Acne Fulminans

Affect youngsters 13 – 17 years of age, very

severe with ulceration and pus discharge,
associated symptoms include (fever, malaise,
myalgia, arthritis and bone pain) laboratory
investigation shows ESR
Can be induced by starting the patient on high
dose of isotretinion (Roaccutane).
Fig 25
 6. Acne Conglobata

Very severe Acne,

Nodulocystic form with abscess formation,
affect Torso more than the face,
usually associated with XYY Syndrome.
 Fig 26

Fig 27
 7. Acne Agminata (Lupus Milliaris
Disseminatus Faciei)

Some believe it is form of Rosacea

(Granulomatous type),
diagnosis is made at Histological base,
Caseating Granulomata at the dermal level.
Fig 28
 8. Acne as part of other syndromes

 MARSH Syndrome
(Melsma, Acne, Rosacea, ,Seborrhoeic eczema, and
Hirsutism)

 Acne Conglobata

 Favre Racouchot syndrome elderly with elastosis as part

of Helioderma, sun exposure is a predisposing factor.

 Polycystic ovarian syndrome

 9. Occupational/
Environmental

 Chloracne rare forms of acne affect patients

exposed to Halogenated Hydrocarbons or
who ingested Chlorinated Phenols (Dioxin)
 I0. Mechanical acne

 Acne excoriee as part of Psychodermatosis

 TREATMENT
Note: All medications used for the treatment of acne act
as:
1. Anti comedonal
2. Anti inflammatory
3. Anti microbial
 Topical Keratolytic

 Retinoid ( Retinoic acid 0.025, 0.05, 0.1%)

 Adapalene (Differin 0.1%)

 Salicylic acid

 Benzoyl peroxide (peeling agent and

antimicrobial)
 Azelaic Acid (10, 15, 20 %)
 Topical Antibiotic

 Topical clindamycin (Dalacin T)

 Erythromycin

 Mupirocin (Bactroban)

 Sodium Fusidic acid (less significant in the

treatment)
 Systemic therapy

 Antibiotic (Macrolides and Tetracylines)

1. Tetracycline
2. Doxycycline
3. Minocycline (blue grey discoloration and
drug induced LE)
4. Azithromycin
 Systemic Retinoids :

 Isotretinoin caps (Roaccutane): 0.5 – 1 mg/kg

 The most effective drug for acne.
 Indicated for
 severe forms (nodulocystic and fulminant)
 for milder forms associated with scarring or
 with significant psychological impact.
 Side effects include:
 cheilitis, dryness, alopecia
 acitretin), photosensitivity,
 xerophthalmia,
 decreased night vision, keratitis,
 benign myalgias.
 intracranialhypertension (incresed risk
with concomitant use of tetracyclines),
photosensitivity,
 hypertriglyceridemia,
hypercholesterolemia,
 elevated liver enzymes,

 depression (controversial),

 skeletal hyperostosis,
 Teratogenicity : Retinoid - induced
embryopathy. Pregnancy category X.
 Pregnancy must be prevented during
treatment and for at least 3 month after
discontinuing the drug.
 Other forms of therapy
 Systemic steroid (Prednisolone): for acne fulminans
and intralesional steriods for cystic acne.
 Photodynamic therapy i.e. Laser therapy and
phototherapy (Less significant)

 Hormonal therapy (Anti-androgen)

Spironolacton (Potassium sparing agent) and
Metformin as (Hypogylcemic agent) in treatment of
PCOS (Polycystic Ovary Syndrome) have good results
on acne
Staph. carriage elimination

 Nasal & perineal care

 Rifampicin 600 mg/d 7-10 days
 Clindamycin 150 mg/d 3 months
 Topical mupirocin