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

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.

Predispositon to 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: obesity, diabetes mellitus, HIV/AIDS,

especially MRSA infection, solid organ transplant recipient,

• Immunodeficiency: cancer chemotherapy, bactericidal defects (e.g., chronic granulomatous disease),

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).

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 – Rheumatic fever, erythema marginatum

• Overgrowth of cornebacterium spp Erythrasma Pitted Keratolysis Trichomycosis

Less commonly, other bacteria may cause skin infections;

• Pseudomonas aeruginosa; wound infections, athlete's foot, gram negative folliculitis, chronic paronychia, spa pool folliculitis and ecthyma gangrenosum

• 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

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.

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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. MANAGEMENTPrevention ;Daily bath. Benzoyl peroxide wash (bar). Check family members for signs of impetigo.

Ethanol or isopropyl gel for hands’and/or involved sites. Treatment of predisposing causes, e.g. pediculosis & scabies.Remove the crusts: by olive oil or hydrogen peroxide.Topical antibiotic ointment;e.g. bacitracin, mupiracin (Bactroban®), Fusidic acid (Fucidin®) 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.

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.

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

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 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 .

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).

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

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 for impetigo lesions: mupirocin, bacitracin, or silver sulfadiazine ointment.

Systemic Antimicrobial Therapy.Adjunctive Therapy Replace significant water and electrolyte loss

intravenously in severe cases.

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.

ERYTHRASMAFrom 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.

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: defects in thickly keratinized skin with eroded pits of variable depth

• Usually asymptomatic. Foot odor.

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.

Scarlet fever (scarlatina)

Age of Onset :Children.

Incidence : Much less than in the past.

Etiology :Usually group A β-hemolytic S.pyogenes (GAS). 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.

Scarlet fever. Evolution of signs and symptoms.

Temp> 38°C

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 desquamationon 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.

• 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.

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.

Cutaneous anthrax A 40-year-old farmer with anthrax.

A. A black eschar at the site ofinoculation with a central hemorrhagic ulceration on the thumb associated with massive edema of the hand.

B. A nodular lymphangitis extending proximally from the primary lesion on the thumb.

SyphilisSynonyms: Lues, the great imitator.

• Syphilis is a human infectious disease caused by the bacterium

Treponema pallidum, it is a very small, spiral bacterium (spirochete) whose form and corkscrew rotation motility can be observed only by dark field microscopy.

• The Gram stain cannot be used, and growing the bacteria is difficult.

Disease transmission ;

• by direct contact with a lesion during the primary or secondary stage.

• in utero by the transplacental route. • during delivery as the baby passes through an infected canal.

Treponema pallidum

Risk of transmission

• The greatest risk of transmission occurs during the primary, secondary, and early latent stages of disease.

• The patient is most infectious during the first 1 to 2 years of infection.

• Patients with secondary syphilis are the most contagious because of the large number of lesions.

• The risk of acquiring syphilis from an infected partner is 10% to 6o%.

• One third of persons with a single exposure to early syphilis will become infected

Primary syphilis

• Incubation period : From 9 to 90 days (average, 21 days) after exposure

• Primary stage= Chancre+ local LN• characterized by a cutaneous ulcer ( chancre),

develops at the site of initial contact.

• Typical chancre; painless , button-like ,single lesion

• regional lymphadenopathy ; Painless , hard, discrete occurs in 1 to 2 weeks.

Secondary syphilis

Secondary syphilis is characterized by : • mucocutaneous lesions, • a flu- like syndrome• generalized adenopathy.

• The types of cutaneous lesions in approximate order of frequency are; maculopapular, papular, macular, annular, papulopustular, psoriasiform, and follicular.

• Lesions occur on the palms or soles in most patients with secondary syphilis

• Temporary irregular ("moth eaten") alopecia of the beard, scalp, or eyelashes may occur .• Moist, anal, wartlike papules (condylomata lata ) are highly infectious . Lesions may appear on

any mucous membrane. • All cutaneous lesions of secondary syphilis are infectious; therefore, if you don't know what it is,

don't touch it. • The differential diagnosis is vast. The commonly observed diseases that may be confused with

secondary syphilis are pityriasis rosea (especially if the herald patch is absent),guttate psoriasis (psoriasis that appears suddenly with numerous small papules and plaques), lichen planus, tinea versicolor, and exanthematous drug and viral eruptions.

• The diagnosis is based primarily on clinical and serologic grounds. • Histologic studies, in the majority of cases, may confirm the disease

Serologic Tests for SyphilisPositive in persons with any treponemal infection (venereal syphilis, endemic syphilis, yaws, pinta). Tests always positive in secondary syphilis.

Nontreponemal STS• Rapid plasma reagin (RPR) test (automated RPR: ART).• VDRL slide test. Measures IgG and IgM directed against cardiolipin-lecithin-cholesterol antigen complex.Non-reactive in 25% of patients with primary syphilis.• In early syphilis: either do fluorescent treponemal antibody-absorbed (FTA-ABS) test or repeat

VDRL in 1–2 weeks if initial VDRLnegative.• Prozone phenomenon: if antibody titer high ,test may be negative; must dilute serum.• Becomes nonreactive or reactive in lower titers following therapy for early syphilis.

Treponemal STS• FTA-ABS test.Agglutination assays for antibodies to T. pallidum :Microhemagglutination assay (MHA-TP; Serodia TPPA test).T. pallidum hemagglutination test (TPHA).• Often remain reactive after therapy; not helpful in determining infectious status of patientwith past syphilis.False-Positive STS. Antigen used in nontreponemal test found in other tissues; may be positive

Causes of False-Positive Reactions in Nontreponemal Serologic Tests for Syphilis

Congenital syphilis

T. pallidum can be transmitted by an infected mother to the fetus inutero.

Risk of transmission:Early maternal syphilis, 75–95%;>2 years’ duration, 35%.• PathogenesisLesions usually develop after fourth month of gestation, associated

with fetal immunologic competence. Pathogenesis depends on immune response of fetus rather than toxic

effect of spirochete. Adequate treatment before 16 week of pregnancy prevents fetal

damage

• TransmissionDuring gestation or intrapartum. Risk of transmission:Early maternal syphilis, 75–95%;>2 years’ duration, 35%.• PathogenesisLesions usually develop after fourth month of gestation,

associated with fetal immunologic competence. Pathogenesis depends on immune response of fetus rather than toxic effect of spirochete.

Adequate treatment before sixteenth week of pregnancy prevents fetal damage.

Untreated: fetal loss up to 40%.

Outcome of pregnancy of a syphilitic mother

• Repeated abortions, after the third month.• Stillborn, premature and macerated fetus.• Full term stillborn infant.• Live born showing signs of congenital syphilis.• Delivery of apparently healthy child, who develops

signs of congenital syphilis after few weeks or months.

• No signs of early congenital syphilis but late congenital syphilis may manifest after few years.

• The child may escape infection & remain healthy for life.

CLINICAL MANIFESTATION

1. Early congenital syphilisAppear before 2 years of age, often at 2–10 weeks. Infectious, resembling severe secondary

syphilis in adult.• Cutaneous: Bullae, vesicles on palms and soles,superficial desquamation, petechiae,

papulosquamous lesions• Mucosal: Rhinitis/“snuffles” (23%); mucous patches, condylomata latum.• Bone changes: osteochondritis, osteitis, periostitis.• Hepatosplenomegaly, jaundice, lymphadenopathy.• Anemia, thrombocytopenia, leukocytosis.2.Late congenital syphilis Appear after 2 years of age. Noninfectious. Similar to late acquired syphilis in adult.• Cardiovascular syphilis.• Interstitial keratitis• Eighth nerve deafness.• Recurrent arthropathy; bilateral knee effusions (Clutton joints). Gummatous periostitis results in destructive lesions of nasal septum/palate.• Asymptomatic neurosyphilis in 33% of patients;clinical syphilis in 25%.

3. Residual Stigmata

• Hutchinson teeth (centrally notched, widely spaced, peg-shaped upper central incisors;

“mulberry” molars (multiple poorly developed cusps).

• Abnormal facies: frontal bossing, saddle nose, poorly developed maxillae, rhagades (linear scars at angles of mouth, caused by bacterial

superinfection of early facial eruption).

• Saber shins.• Nerve deafness• Old chorioretinitis, optic atrophy, corneal opacities due to interstitial keratitis.

Hutchinson teeth

• The drug of choice in the treatment of syphilis is benzathine penicillin G

Recommendations for the Treatment of Syphilis