1. Bacterial
infections
Dr Qassim S. Al-Chalabi
F.A.B.H.S

2. Bacterial infections The normal skin flora
Protects the skin from bacterial infections through bacterial interference.
The resident skin flora consists of:
Staphylococcus species, e.g. S. hominis & S. epidermidis. Staph. aureus isn’t a member of resident skin flora except in anterior nares or perineum (in 20% of individuals) & in lesional skin of atopic dermatitis (90% of pts).
- Micrococcus species Aerobic coryneforms.
- Anaerobic propionibacterium species, e.g. P. acnes. commonly inhabit the sebaceous hair follicles.
- Yeasts: pityrosporum.

4. Impetigo contagiosum
Acute contagious superficial pyogenic infection of the skin.
Staph. Aureus and Streptococcus Pyogens are the most common cause of skin infections.
Impetigo occurs most frequently in early childhood, although all ages may be affected. It occurs in the temperate zone, mostly during the summer in hot, humid weather.

5. Predisposing factors for pyoderma
Common sources of infection for children are pets, dirty fingernails, and other children in schools, daycare centers, or crowded housing areas; for adults, common sources include infected children and self-inoculation from nasal or perineal carriage.
Impetigo often complicates pediculosis capitis, scabies, herpes simplex, insect bites, eczema, and other itching skin diseases.
IMP

6. 1- Non-bullous impetigo
Staph. aureus or group A stretp. or both “mixed infections”.
May arise as 1ry inf. or as 2ry inf. of pre-existing dermatoses, e.g. pediculosis, scabies & eczemas.
An intact st. corneum is probably the most important defense against invasion of pathogenic bacteria.

7. Clinical feature
A thin-walled vesicle on erythematous base, that soon ruptures & the exuding serum dries to form golden-yellowish (honey-color) crusts that dry & separate leaving erythema which fades without scarring.
Regional adenitis with fever may occur in severe cases.
Sites: face & scalp (in pediculosis). Any part could be affected except palms & soles.
Complications: Post-streptococcal acute glomerulo-nephritis “AGN” especially in cases due to strepto. Pyogenes

9. Site: more on distal extremities (thighs & legs).
Non-bullous impetigo – varieties (Cont’d)
Ecthyma (ulcerative impetigo): adherent crusts, beneath which purulent superficial saucer-shaped ulcer occur. Healing occurs after few wks, with scarring.
Site: more on distal extremities (thighs & legs).

11. SSSS (Cont’d)
Treatment of impetigo
1. Treatment of predisposing causes, e.g. pediculosis & scabies.
2. Remove the crusts: by olive oil or hydrogen peroxide or soap and water.
3. Topical antibiotic ointment, e.g. tetracycline, bacitracin, mupiracin (Bactroban®), Fusidic acid (Fucidin®).

12. Azithromycin caps 500 mg daily for 3 days in adults.
SSSS – treatment (Cont’d)
4. Systemic antibiotics are indicated especially in the presence of fever or lymphadenopathy, in extensive infections involving scalp, ears, eyelids or if a nephritogenic strain is suspected, e.g. penicillin, erythromycin & cloxacillin.
Azithromycin caps 500 mg daily for 3 days in adults.
In erythromycin-resistant S. aureus: amoxicillin + clavulanic a. (Augmentin®) 25 mg/kg/day.

13. 2- Bullous impetigo
Staph. aureus through staphylococcal toxin (exfoliatin).
Age: all ages, but more common in childhood & newborn.
The bullae are less rapidly ruptured (persist for 2-3 days) & become much larger. The contents are at first clear, later cloudy, after rupture thin, brownish crusts are formed.
Site: face is often affected, but the lesions may occur anywhere, including palms & soles.

16. Syndromes caused by staph. exotoxins
Staph. Scalded Skin Syndrome “SSSS” (Ritter’s dis.)
It occurs mainly in infancy & childhood or rarely in adults with renal failure or immunological incompetence.
The condition is usually caused by a toxin produced by staphylococcal infection elsewhere (e.g. impetigo or conjunctivitis). Staph. aureus of phage group II, mostly type 71, which elaborates two exotoxins, epidermo-lytic toxins A & B (ET-A & ET-B).

17. SSSS (Cont’d)
Clinically
it begins suddenly with diffuse, tender, red skin simulating “scald”. Large flaccid bullae occur  rupture immediately. Large sheets of superficial epidermis separate & exfoliate. Healing occurs usually within 7-14 days with or without treatment. Usually good prognosis.

19. Treatment (good prognosis)
SSSS – clinically (Cont’d)
Treatment (good prognosis)
Systemic & topical antibacterial agent:to  secondary infection.
Supportive treatment: iv fluid, electrolyte disturbance.

20. Erysipelas
It’s due to infection of the dermis & upper subcutaneous tissue by group A streptococci.
The organism reaches the dermis through a wound or small abrasion.
Site : Leg & face.
It begins with high fever & rigors. There is a well-demarcated erythematous, hot, tender swelling of the skin. The surface may show vesicles or bullae. Lymphangitis & lymphadenopathy are frequent.

22. Complications Recurrences may lead to lymphedema.
Erysipelas (Cont’d)
Complications
Recurrences may lead to lymphedema.
Subcutaneous abscess.
Septicemia.
Nephritis.

23. Cellulitis
It is an acute inflammation of subcutaneous tissue. Currently, erysipelas is regarded as a form of cellulitis rather than a distinct entity.
Cellulitis is usually caused by gp A strept., but staph. aureus may be implicated.

24. Cellulitis (Cont’d)
Clinically: the edge is diffuse with indurated, red, tender area of the skin.
Recurrent strept. cellulitis or erysipelas is due to lymphatic damage & venous insufficiency.
Treatment of erysipelas & cellulitis :
Systemic antibiotics, especially penicillin, e.g. benzyl penicillin mg IV/6 hrs or erythromycin.
Rest, analgesics

25. Folliculitis
= inflammatory disease of the hair follicles, which may be infectious or non-infectious.
Superficial folliculitis
It isn’t always infective in origin, physical or chemical injury or adhesive plasters may be associated with folliculitis, usually sterile.

27. Superficial folliculitis (Cont’d)
1. Follicular impetigo of Bockhart: a dome-shaped pustule at the orifice of a hair follicle that heals within 7-10 days. Topical steroids are a common predisposing factor.
2. Pseudofolliculitis of the beard: from penetration into the skin of sharp tips of shaved hairs.

30. Deep folliculitis 1. Sychosis “Folliculitis barbae”
Red follicular papules or pustules centered on a hair, usually remain discrete over the beard or upper lip, but may coalesce to produce raised plaques studded with pustules later will be scaring and hair loss.
DD: pseudofolliculitis of the beard, Tinea barae.

32. Deep folliculitis (Cont’d)
2. Furunculosis “Boils”
It is a staphylococcal infection similar to, but deeper than folliculitis & invades the deep parts of the hair folliculitis.
Occasionally several closely grouped boils will combine to form a carbuncle. The carbuncle usually occurs in diabetic cases. The site of predliction is the back of the neck.

34. Other causes of folliculitis
Gram negative folliculitis with antibiotic treatment of Acne Vulgaris.
Pityrosporum folliculitis.
Eosinophilic folliculitis in HIV infections.
Pseud. aeruginosa folliculitis.

35. Hidradenitis suppurativa “Apocrinitis”
is a chronic disease characterized by recurrent abscess formation, primarily within the folded areas of skin that contain both terminal hairs and apocrine glands.
It begins after puberty, commonly in females.
Sites: axillary & anogenital regions where apocrine glands are present. There is small red, tender, subcutaneous nodules that become fluctuant, becomes chronic & indolent due to subcutaneous extension. Rupture & sinuses discharging pus occur. Healing occurs with scar formation.

37. Treatment Hidradenitis suppurativa (Cont’d)
Appropriate antibiotics for 2 wks, e.g. erythromycin and metronidazole or clindamycin or long term of tetracyclines.
Systemic corticosteroids, e.g. prednisolone 60 mg daily.
Oral contraception containing 50 mg ethyl estradiol may be useful.
Isotretinoin for 4 months .
Surgery in refractory resistant cases.

38. Erythrasma
It is chronic, localized superficial infection of skin by Corynebacterium Minutissimum
There is sharply-defined but irregular brown, scaly patches usually localized to groins, axillae, toe clefts or may cover extensive areas of trunk & limbs. Obesity & DM may coexist.
It gives coral-red fluorescence under Wood’s light.
Topical treatment with antifungal agents for 2 weeks or topical fusidic acid.
Erythromycin orally.

41. Trichomycosis axillaris
• Causative organism: Corynebacterium tenuis
• Characteristic features: Yellowish brown concretions on axillary hair shafts
• Treatment: Shaving; topical erythromycin.

43. Pitted keratolysis
The combination of unusually sweaty feet and occlusive shoes encourages the growth of organisms that can digest keratin. The result is a cribriform pattern of fine punched-out depressions on the plantar surface, coupled with an unpleasant smell.

45. Anthrax (Malignant Pustule)
Acute disease in humans and animals caused by Bacillus anthracis , a Gram-positive spore-forming rod.
Primarily caused by contact with infected wild or domestic animals, or their products (e.g., wool, goat, animal hides, bones, etc.)

46. Clinical picture Clinical forms: cutaneous, pulmonary, and GI.
IP= ultra short 1-5 days patients may experience low-grade fever and malaise
Primary lesion is a “malignant pustule,” which begins as a painless papule, evolves into a hemorrhagic bulla with surrounding nonpitting edema, and ultimately forms a characteristic black eschar surrounded by vesicles.
Regional lymph glands become tender an enlarged, and frequently suppurate.

48. Treatment: (i) Bioterrorism associated: ciprofloxacin or doxycycline
(ii) Conventional anthrax: Penicillin