1. Bacterial skin infections
DR. Ali El-ethawi
Specialist Dermatologist
M.B.CH.B , F.I.C.M.S, C.A.B.D
5th class lecture

2. The normal skin flora
• Normal skin is heavily colonized by bacterial flora (harmless
commensals) such as;
• coagulase negative staphylococci (e.g; S. epidermidis) .
• Micrococcus species.
• Aerobic coryneforms.
• Anaerobic propionibacterium species, e.g. P. acnes, P.
granulosum, commonly inhabit the sebaceous hair follicles.
• Yeasts, pityrosporum
• Protects the skin from bacterial infections through bacterial
interference.
• Colonization is more dense in ;intertriginous and occluded sites.

3. Predisposition to skin infection
• Chronic S. aureus carrier state (nares, axillae,perineum,
vagina)
• Warm weather/climate, high humidity
• Skin disease, especially atopic dermatitis, familial
pemphigus
• Social situation: poor hygiene, crowded living conditions,
neglected minor trauma
• Chronic disease:, diabetes mellitus, HIV/AIDS, solid
organ transplant recipient & obesity
• Immunodeficiency, bactericidal defects (e.g., chronic
granulomatous disease)& cancer chemotherapy

4. Bacteria cause disease by
• direct invasion of tissues,
• by secreting toxins,
• by causing immunologic consequences
that result in disease.
Bacteria, like viruses, may also sometimes result in exanthems (rashes).

5. The most common bacteria to cause skin
infections are
• Staphylococcus aureus ;
– Impetigo (school sores)
– Folliculitis
– Furunculosis (boils)
– Staphylococcal scalded skin syndrome
– Toxic shock syndrome
– Botryomycosis (pyoderma vegetans)
Streptococcus pyogenes
– Cellulitis
– Erysipelas
– Impetigo
– Necrotising fasciitis
– Scarlet fever
• Overgrowth of cornebacterium spp
Erythrasma
Pitted Keratolysis
Trichomycosis

6. Less commonly, other bacteria may cause skin
infections;
• Pseudomonas aeruginosa;
wound infections, athlete's foot, gram negative folliculitis, chronic paronychia, spa pool follic
• Erysipelothrix insidosa, cause of erysipeloid (usually an animal infection)
• treponema species cause syphilis (STD) , yaws and pinta
• Hemophilus species ;, cause of chancroid (STD) and cellulitis in young children
• Neisseria species, cause of gonorrhoea (STD) and meningococcal disease .
• Calymmatobacterium granulomatis ; granuloma inguinale (STD)
• Klebsiella rhinosclermatis; cause of rhinoscleroma
• Bacillus anthracis ; anthrax
• Clostridium perfringens and other species cause gas gangrene
Calymmatobacterium granulomatis, cause of granuloma inguinale

7. IMPETIGO AND ECTHYMA
Etiology: S. aureus; also, group-A streptococci (GAS)
Infections of the epidermis (impetigo),
Infections which may extend into the dermis (ecthyma)
Clinical findings:
▪ Impetigo: crusted erosions
▪ Ecthyma: crusted deep erosions or ulcers.
Impetigo is a common, contagious, superficial skin infection that is produced by streptococci,
staphylococci, or a combination of both bacteria
There are two different clinical presentations:
bullous impetigo (primarily a staphylococcal disease)
nonbullous impetigo. a streptococcal disease,
but staphylococci are isolated from the majority of lesions in both bullous and nonbullous impetigo
C/F : Both begin as vesicles with a very thin, fragile roof consisting only of stratum corneum. And may
become pustular before rupturing to leave extending area of exudation & yellow crusting
Symptoms of itching and soreness are mild; systemic symptoms are infrequent.
.

9. impetigo
Impetigo may occur as 1ry inf. after a minor skin injury such as an insect bite or as 2ry inf. of
pre-existing dermatoses, e.g. pediculosis, scabies & eczemas.
course ;The disease is self-limiting, but when untreated it may last for weeks or months.
complication; Post -streptococcal glomerulonephritis may follow impetigo.
MANAGEMENT
Treatment of predisposing causes, e.g. pediculosis & scabies.
Remove the crusts: by olive oil or hydrogen peroxide.
Topical antibiotic ointment;
e.g. bacitracin, mupiracin or Fusidic acid
Systemic antibiotics; e.g. penicillin, erythromycin & cloxacillin.
are indicated especially in the presence of
• fever
• lymphadenopathy,
• in extensive infections involving scalp, ears, eyelids
• if a nephritogenic strain is suspected.

13. Ecthyma
• is characterized by ulcerations that are covered by adherent crusts.
• Poor hygiene is a predisposing factor.
• Ecthyma has many features similar to those of impetigo But it heal with scarring
• Distribution : more common on distal extremities.

14. Furuncle and Carbuncles
Furuncle (abscess or boil) ;is a walled-off collection of pus
that is a painful, firm, or fluctuant mass.
Carbuncles ;are aggregates of infected hair follicles.
The infection originates deep in the dermis and the subcutaneous tissue, forming a
broad, red, swollen, slowly evolving, deep, painful mass that points and drains
through multiple openings.
Malaise, chills, and fever precede or occur during the active phase.
Deep extension into the subcutaneous tissue may be followed by sloughing and
extensive scarring.
Sites ; Areas with thick dermis (i.e., the back of the neck, the back of the
trunk, and the lateral aspects of the thighs) are the preferred sites.
Treatment ;of an abscess, furuncle, or carbuncle is incision and drainage plus
systemic antimicrobial therapy

16. ERYSIPELAS AND CELLULITIS
• Acute, spreading infections of dermal and subcutaneous tissues
• Characterized by a red, hot, tender area of skin
• In most instances there is fever and leukocytosis .
• Both may be accompanied by lymphangitis and lymphadenitis.
• Often originating at the site of bacterial entry
• Erysipelas involves the superficial layers of the skin and cutaneous
lymphatics; cellulitis extends into the subcutaneous tissues.
• Caused most frequently by group A streptococcus (erysipelas) or S.
aureus .
• Cellulitis is differentiated clinically from erysipelas by two physical findings:
cellulitis lesions are primarily not raised, and demarcation from uninvolved
skin is indistinct.
• Erysipelas ;if untreated ,the condition can even be fatal ,but it responds
rapidly to systemic pencillin ,some times given intravenously
• Treatment of cellulites; is elevation , rest -sometime in hospital – and
systemic antibiotics, sometimes given intravenously .

20. Staphylococcal scalded skin syndrome
(SSSS)
Etiology: S. aureus.
Age: occurs mainly in newborns and infants < 2years.
Also, older immunocompromised persons
Pathogenesis: toxin-mediated epidermolytic disease.
Clinical syndromes: Erythema and widespread
detachment of the superficial layers of the epidermis,
resembling scalding
D. Dx; TSS, Kawasaki syndrome, drug-induced
toxic epidermal necrolysis (TEN).

21. painful, tender, diffuse erythema was followed by generalized epidermal
sloughing and erosions.
S. aureus had colonized the nares with perioral impetigo, the site of exotoxin
production.

24. Management:
Prophylaxis ; Prevent spread of toxigenic S.aureus in neonatal care
units.
General Care Hospitalization is recommended for neonates and young
children.
Topical Therapy Baths or compresses for debridement of necrotic
superficial epidermis.
Topical antimicrobial agents; like for impetigo lesions: mupirocin,
bacitracin, or silver sulfadiazine ointment.
Systemic Antimicrobial Therapy.
Adjunctive Therapy Replace significant water and electrolyte loss
intravenously in severe cases.

25. TOXIC SHOCK SYNDROME (TSS)
Etiology: Toxin-producing S. aureus and GAS
Clinical setting
▪ Staphylococcal TSS
• Menstrual (MTSS) (rare after 1984)
• Non menstrual (NMTSS)
▪ Streptococcal TSS
Clinical manifestations
▪ Rapid onset of fever and hypotension
▪ Skin findings
• Early: generalized skin and mucosal erythema
• Late: desquamation in early convalescence
▪ Organ hypoperfusion and multisystem failure
Management: systemic antibiotic to treat infection and stop toxin production.
Irrigation of the infected site are needed .
Supportive RX.

26. ERYTHRASMA
From the Greek: “red spot”
Age of Onset ; Adults
Etiology: Corynebacterium minutissimum
Distribution: intertriginous areas of webspaces of feet, groins, axillae,
submammary areas
Clinical findings: well-demarcated red or tan patches, ± scale
D.DX; from dermatophytosis and noninfectious intertrigo
Diagnosis: Clinical findings, absence of fungi on direct microscopy, positive
Wood lamp examination( shows coral red fluorescence )
Prevention/Prophylaxis,
Topical antiseptic alcohol gels: isopropyl, ethanol.
Topical Therapy Preferable.
Topical erythromycin or clindamycin solution twice daily for 7 days.
Sodium fusidate ointment, mupirocin ointment or cream.
Topical antifungal agents; clotrimazole,.
Systemic Antibiotic Therapy ; A macrolide or a tetracycline for 7 days.

28. PITTED KERATOLYSIS
• Etiology: Kytococcus sedentarius
• Age of onset: young adults.
• Sex: males > females.
Distribution: plantar feet, web spaces of feet
Predisposition: hyperhidrosis and Occlusive footwear
• Clinical findings: eroded pits of variable depth occur as defects in thickly
keratinized skin
• Usually asymptomatic , but with Foot odor.

29. TRICHOMYCOSIS
Etiology: Corynebacterium ;gram-positive diphtheroid.
age &sex ; adults, males > females.
Distribution: axillae (trichomycosis axillaris),
pubic hair (trichomycosis pubis)
Predisposition: hyperhidrosis
Clinical findings:
granular concretions (yellow, black, or red) on hair shaft.
Hair appears thickened, beaded, firmly adherent.
Insoluble adhesive may erode cuticular and cortical keratin.
Management:
shave off affected hair.
Benzoyl peroxide wash.
Alcohol gel.
Topical erythromycin or clindamycin.

31. Scarlet fever (scarlatina)
Age of Onset :Children.
Incidence : Much less than in the past.
Etiology :Usually group A β-hemolytic S. pyogenes . Uncommonly,
ET-producing S. aureus.
• Incubation Period : Rash appears 1–3 days after onset of
infection.
• PRODROMAL AND ERUPTIVE PHASE .
The sudden onset of fever and pharyngitis is followed shortly by
nausea, vomiting, headache, and abdominal pain.
• enlarged cervical lymph nodes .

32. Scarlet fever.
Evolution of signs and symptoms.
Temp
> 38°C

33. Exanthem (skin rash)
Face: flushed with perioral pallor.
• Initial punctate lesions become confluently erythematous, i.e., scarlatiniform (Numerous
papules giving a sandpaper-like texture to the skin.)
• Palms/soles usually spared.
• Linear petechiae (Pastia sign) occur in body folds.
• Tongue
• White tongue: Initially is white with scattered red, swollen papillae (white strawberry
tongue).
• Red strawberry tongue: By the fourth or fifth day, the hyperkeratotic membrane is
sloughed, and the lingular mucosa appears bright red.
Desquamation: Exanthem fades within 4–5 days and is followed by desquamation
on the body and extremities and by sheet-like exfoliation on the palms/fingers and
soles/toes.
In subclinical or mild infections, exanthem and pharyngitis may pass unnoticed.
In this case patient may seek medical advice only when exfoliation on the hand and soles
is noted.

36. • MANAGEMENT
• Symptomatic Therapy Aspirin or acetaminophen for fever and/or
pain.
• Systemic Antimicrobial Therapy Penicillin is the drug of choice
because of its efficacy in prevention of rheumatic fever. Goal is to
eradicate GAS throat carriage.
• Others: cephalosporins, erythromycin , or the newer macrolides.
• Follow-Up Re-culture of throat recommended for individuals with
history of rheumatic fever or if a family member has history of
rheumatic fever.

37. CUTANEOUS ANTHRAX
Synonym : Malignant pustule
Etiology: Bacillus anthracis
Zoonosis
Pathogenesis: toxin-mediated
Portal of entry:
▪ Skin: cutaneous abrasions
▪ Inhalations (woolsorters’ disease)
▪ Ingestion
Cutaneous anthrax accounts for 95% of anthrax cases in United States
Clinical findings of cutaneous anthrax:
▪ Black eschar surrounded by edema and purple vesicles
• Management: Cutaneous anthrax can be self-limited, but antibiotic therapy is
recommended.
• Drug of choice :
• Ciprofloxacin, 400 mg IV q12h, or doxycycline,100 mg IV q12h, is optimal.
Alternatives : None.
• Surgery for excision of eschar is contraindicated.