BACTERIAL

Dr. Rasha Turky Ass. Prof of Dermatology, Andrology and STDs

The Skin

 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. Normal Skin Flora

Major bacterial groups  Coryneforms (Gram +ve)  Staphylococci (Gram +ve cocci, aerobs)

Minor bacterial groups  Acinetobacter (25%) Gram –ve Bacilli  Micrococcus Skin Infections  The skin always has some amount of bacteria, fungus and viruses living on it.

 Infections occur when there are breaks in the skin and the organisms have uncontrolled growth.

Staph. Aureus Infection

1. Direct infection of skin: , , , furunculosis, , sycosis.

2. Secondary infection: eczema, infestations, ulcers, …etc.

3. Effect of bacterial toxin: staph.-associated scalded skin syndrome (SSSS), . Streptococcal Infection (gp A streptococci)

1. Direct inf. of skin or subcut. tissue: Impetigo, ecthyma, , vulvovaginitis, perianal inf., ulcers, blistering, .

2. 2ry inf.: eczema, infestations, ulcers, …etc. Tissue damage from circulating toxin: , toxic shock-like syndrome.

3. Skin lesions attributed to allergic hyper-sensitivity to strepto. antigens: erythema nodosum, vasculitis.

4. Skin dis. provoked or influenced by strepto. inf.: psoriasis.

Impetigo  It is acute contagious skin infection caused mostly by staph. Aureus and strept. It affects children mainly, esp. in summer.

 Clinical types: .

1- Non-: Caused by staph., strept. or both organisms.

2- Bullous impetigo: Caused by staph aureus Non- Bullous Impetigo

 Staph. aureus or gp 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 . Clinical picture  A thin-walled vesicle on erythematous base, that soon ruptures & the exuding serum dries to form yellowish-brown (honey-color) crusts that dry & separate leaving erythema which fades without scarring.

 Regional adenitis with fever may occur in severe cases.

 Sites: Exposed parts eg. face & extremities. Scalp. Any part could be affected except palms & soles.

 Complications: Poststreptococcal acute glomerulonephritis ―AGN‖ especially in cases due to strepto. Pyogenes. Varieties  Circinate impetigo: with peripheral extension of lesion & healing in the center.

 Crusted impetigo: on the scalp complicating pediculosis. Occipital & cervical Lymph node are usually enlarged & tender.

 Ecthyma (ulcerative impetigo): adherent crusts, beneath which purulent irregular ulcers occur. Healing occurs after few weeks, with scarring. More on distal extremities (thighs & legs).

Bullous Impetigo  Age: all ages, but commoner in childhood & newborn (impetigo neonatorum).

 Site: face is often affected, but the lesions may occur anywhere, including palms & soles.

 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.

Treatment of Impetigo  Treatment of predisposing causes: e.g. eczema, pediculosis & scabies.

 Remove the crusts: by olive oil or hydrogen peroxide.

 Topical antibiotic: e.g. 2% mupirocin, Gentamycine, Fucidic acid, tetracycline.

 Oral amoxacyllin or Ampicillin can also be used.

 In cases, with an allergy to penicillin, erythromycin can be given.

Folliculitis  It is inflammatory disease of the hair follicles, which may be infectious or non-infectious.

Superficial Folliculitis (Bockhart’s Impetigo)

 A dome-shaped pustule at the orifice of a hair follicle that heals within 7-10 days.

 Caused by staph aureus and affects mainly extremities and scalp.

 Topical steroids are a common predisposing factor. Sycosis barbae  Recurrent 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.

 The irritation is caused by deep infection of hair follicles often by Staph. Aureus.

Psudofolliculitis

 It is inflammation of the hair follicles and surrounding skin caused from penetration of sharp tips of shaved hairs into the skin.

Management of folliculitis

 Avoid greasy applications on the skin.

 Topical antibiotic can be used.

 Systemic antibiotics: Cloxacillin or erythromycin is choices of treatment. Hidradenitis Suppurativa  HS is a chronic cutaneous disorder that targets apocrine gland-bearing skin sites, in particular the axillae and anogenital region.

 It is characterized by recurrent ―‖ and draining sinus tracts with subsequent scarring.

 Starts at or soon after puberty.

 Children are not affected unless they have precocious puberty, and women are affected three times as often as men.

Pathogenesis  AD (familial form).  Caused by follicular occlusion.  Hyper-androgenism doesn’t play a role in HS.  Bacteria are secondly colonize, which may exacerbate HS.  An underlying immunologic aberration.  Defect in inflammatory mediators and receptors to apoptosis.  Enhanced expression of TLR2 within macrophages and DCs.  Mechanical irritation before onset of the disease.  Smocking and obesity are strongly associated with the disease and may exacerbate it. Treatment  General measure: avoidance of tight clothes, reassurance, analgesic, weight loss, smocking cessation.  Antibiotic:  Topical clindamycin 1 % solution twice daily for 12 weeks.  Tetracycline 500 mg twice daily for more than 3 months.  Combination of oral clindamycin and rifampcin.  Minocycline.  Dapson: 25—150 mg daily.  Retinoids: isotrtinoids 0.5 mg/kg/day for 4-6 months.  Hormones: antiandrogen???.  Immunosuppressive and antiinflammatory agents: prednisone 5 mg ever other day, tarolimus 1 mg daily, Myclphenolate mofetil, azathioprime, methyl prednisone and MTXs.  TNF-alph (infliximab)  Neurotoxins (BT) may reduce apopcrine gland secretion.  Physical TTT: raDIOTHERAPY, LIGHT, Radiofrequency, cryosurgery, CO2 laser.  Surgery for intractable HS. Follicular occlusion triad - Acne conglobata. - HS. - Dissecting cellulitis of the scalp.

Follicular Occlusion Tetrad Follicular occlusion triad + pilonidal sinus Frunculosis/ Frunculosis/  It is a that invades the deep parts of the hair folliculitis (deeper than folliculitis).

 A furuncle or boil is a round, tender, circumscribed, perifollicular inflammation, which generally tends to suppurate.

 Discharge pus and heal with scar formation.

Carbuncles  Carbuncle is an infection involving subcutaneous tissue around several hair follicles.

 Combination of several closely grouped boils will combine to form a carbuncle.

 It usually occurs in diabetic cases or malnourished cases.

 The site of election is the back of the neck.  Painful suppuration begins after 5-7 days of infection.

 Pus discharge occurs from multiple follicular orifices.

 Followed by necrosis of the intervening skin leaving large deep ulcer.

FURUNCLE CARBUNCLE Treatment  Preventive measures are very important especially to prevent recurrence of infection from nasal foci, autoinoculation, from peri- anal areas.

 Avoid squeezing, irritation and trauma to the lesions.

 Treatment of the colonized areas and the primary focus as in nostrils.

 Topical antibacterial cream such as Muperacin cream which when applied twice daily in the nostril for one week will eradicate colonized micro-organism for 6 months.

 Using a suitable anti septic soap may have some good effect. Cellulitis and Cellulitis  Cellulitis is an Acute/Sub-acute/Chronic infection of subcutaneous tissues.

 Commonly caused by Streptococcal (Group A), Staphylococci and rarely clostridia.

 The affected skin appears swollen, red, tender and warm with ill-defined border.

 Usually affect skin of the L.L but can occur in the face, arms and other areas.

 It occurs when bacteria entered through a cracked or broken skin.

 If left untreated, the infection can spread to the L.N and blood stream and rapidly become life- threatening.

 Differential Diagnosis: DVT.

Treatment  Cold application: to relief local discomfort.  Analgesic to relief pain.  Treat the fever and pain and elevate the affected part.  Crystalline penicillin or procaine penicillin is the first line therapy.  Oral Ampicillin or Amoxicillin may be used for mild infection and after the acute phase resolves.  Appropriate Antibiotic, according to culture: Erythromycin, Augmentin. Cellulitis Erysipelas  It’s due to infection of the dermis & upper subcutaneous tissue by gp A streptococci.

 The organism reaches the dermis through a wound or small abrasion. It is regarded as a superficial ―dermal‖ form of cellulitis.

 Usually begins on the face or a lower extremity.

 There is pain, superficial erythema, and plaque-like edema with a sharply defined margin (Boarder easily palpable).

 Fever and malaise may precede local signs.

 Blistering and hemorrhage may occur.

are frequent.

Complications:  Recurrences may lead to lymphedema.  Subcutaneous .  Septicemia.  Nephritis.

 Treatment:  Systemic antibiotics, especially penicillin, e.g. benzyl penicillin (600- 1200 mg IV/6 hrs)

 Rest, analgesics.

Erysipelas Edge of the lesion: well demarcated and raised in erysipelas and diffuse in cellulitis. Skin Diseases related to Coryneform Bacteria Erytherasma  It is mild, chronic, localized superficial infection of skin by Coryn. Minutissimum.

 Clinically: 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.

 Coral red fluorescence under wood’s light.

 Treated topically with azole antifungal agents for 2 weeks or topical fucidin. Erythromycin orally.

Pyonychia

 It is acute erythematous swelling of proximal and lateral nail fold.

 Painful.

 Treatment: Drain Pus, Antibiotic, Analgesic. Staphylococcal scalded skin syndrome (Ritter’s disease)

 SSSS is primarily a disease of infants and young children, with decreased renal toxin clearance (especially neonates) and/or lack oftoxin-neutralizing antibodies.

 A severe reaction to S. aureus strains producing toxins (exfoliative toxin also know as epidermolytic toxins (ETs).

 ETs bind and cleave desmoglein 1 (Dsg1) → splitting of the desmosomes → disruption of the epidermal granular layer and bulla formation.

Clinical picture  Prodromal symptoms of malaise, fever, irritability and severe tenderness of the skin.

 Erythema typically first appears on the head (accompanied by facial edema) and in intertriginous sites, often with generalization within 48 hours.

 The skin subsequently develops a wrinkled appearance owing to the formation of flaccid, sterile bullae within the superficial epidermis.

 Positive Nikolsky sign.

 No Intraoral lesions.  Classically, the flexural areas are the first to exfoliate, leaving moist skin and thin crusting.

 Patients demonstrate characteristic periorificial (e.g. perioral, periocular) crusting and radial fissuring.

 Scaling and desquamation continue for the next 3–5 days, followed by re-epithelialization without scarring.

 With proper treatment, SSSS resolves in 1–2 weeks, usually without sequelae.

 The mortality rate is 3% for children but >50% in adults.  Histologic examination shows a sharply demarcated zone of cleavage at or below the stratum granulosum. There are usually no inflammatory cells in the bullae. The upper dermis also lacks an inflammatory infiltrate.

 Treatment  Hospitalization and parenteral antibiotics.  Oral treatment with a β-lactamase-resistant antibiotic (e.g. dicloxacillin, cephalexin) for a minimum of 1 week is usually sufficient for milder disease.  Identification and decolonization of S. aureus carriers.

Toxic shock syndrome  TSS is due to infection or colonization with strains of S. aureus that produce toxic shock syndrome toxin-1 (TSST-1).

 This toxin is thought to act as a ―superantigen‖ that binds to MHC-II molecules of APCs and to T-cell receptors in a non antigen-specific manner→ massive release of cytokines and chemokines as well as clonal T- cell expansion.

 Neonatal TSS-like exanthematous disease occurs during the first week of life due to colonization with TSST-1-producing S. aureus with a mild course due to the immature, relatively anergic state of T cells in newborns. Clinical picture

 Sudden onset of high fever with myalgias, vomiting, diarrhea, headache and pharyngitis.

 Rapid progression to hypotensive shock can occur.

 The clinical spectrum ranges from relatively mild to fulminant fatal disease.

 Skin manifestations are more extensive in staphylococcal TSS than in streptococcal TSS.

 Patients usually develop diffuse erythema or a scarlatiniform exanthem that starts on the trunk and spreads to the extremities.  Erythema and edema of the palms, soles and oral mucosa as well as a strawberry tongue, hyperemia of the conjunctivae.

 With disease progression, generalized non-pitting edema occurs.

 Desquamation of the hands and feet occurs 1–3 weeks after the onset of symptoms.

 After recovery, Beau’s lines and nail shedding can be seen.

 In severe cases, telogen effluvium may occur.

 Biopsy shows an infiltrate of neutrophils and lymphocytes in the superficial dermis. Papillary dermal edema as well as epidermal spongiosis and exocytosis may be noted.

 Treatment:  Intensive monitoring and supportive therapy in sever cases  Hypotension treated with intravenous fluids and vasopressor agents.  Beta-lactamase resistant antibiotics are used to eradicate the toxin-producing staphylococci.  Some advocate using antibiotics that suppress protein (and thereby toxin) production, such as clindamycin.  Administration of intravenous immunoglobulin (IVIg) may help to neutalize the toxin.  In severe cases of shock unresponsive to antibiotics, low- dose corticosteroids have been used.

Scarlet Fever  Primarily a disease of children, scarlet fever.

 The erythematous exanthem and enanthem are due to toxins produced by group A β-hemolytic streptococci.

 Caused by streptococcal pyrogenic exotoxins (SPEs) types A, B and C (also referred to as erythrogenic toxins), which are produced by group A streptococci and lead to immune activation.

 Scarlet fever usually follows tonsillitis or pharyngitis.  Scarlet fever typically preceded by the sudden onset of a sore throat, headache, malaise, chills, anorexia, nausea and high fevers.

 Young children, may experience vomiting, abdominal pain and seizures.

 The eruption begins 12–48 hours later as blanchable erythema on the neck, chest and axillae.

 Subsequent generalization (usually within 12 hours) and development of tiny superimposed papules with a sand paper-like texture (―sunburn with goose ‖).  Pastia’s lines (linear petechial streaks) are seen in the axillary, antecubital and inguinal areas.

 The cheeks are flushed with circumoral pallor.

 The throat is red and edematous, developing an exudate after 3–4 days; palatal petechiae and tender cervical adenopathy are often evident.

 The tongue is initially white with bright red papillae, but later becomes beefy red (―strawberry tongue‖).

 Desquamation occurs after 7–10 days, most prominently on the hands and feet (see Fig. 74.8A&B), and can last for 2–6 weeks  Penicillin (or amoxicillin) is the drug of choice; a 10– 14-day course is usually sufficient.

 A clinical response can be expected within 24–48 hours.

 Antibiotic treatment as long as 10 days after the onset of symptoms will prevent the development of rheumatic fever.

 In penicillin-allergic patients, a first-generation cephalosporin, clindamycin or a macrolide can be used.

Necrotizing Fasciitis  Necrotizing fasciitis is uncommon rapidly progressive necrosis of subcutaneous fat and fascia, with relative sparing of underlying muscles.

 Rapidly fatal unless recognized quickly and treated aggressively.

 Risk factors: DM, immunosuppression, IV drug abuse, hypertension, obesity/malnutration.

 May involve extremities, trunk, neck, face pernium and genitalia (Fournier’s ).

Clinical Picture

 Early in the course, the area become hot, red and edematous.

 Within 2-4 days the affected area become bluish-black with an irregular ill-defined border and usually hemorrhagic bullae and foul- smelling discharge. Treatment  Extensive surgical debridement (fasciotomy) is the mainstay of effective treatment. Occasionally, amputation may be needed.

Therapy should be initiated with a β-lactam/β-lactamase inhibitor with broad-spectrum coverage against streptococci, staphylococci, Gram-negative bacilli and anaerobes.

 IVIg may be useful for patients with severe group A streptococcal infection.

 Nutritional support is crucial for enhancing postoperative wound healing.

 Reconstructive surgery is often necessary.  It is bacterial infection seen in people who handle raw meat (especially pork) and Fish.

 Organism get entry through breaks in the skin.

 Common on fingers, hand or forearms.

 No systemic symptoms.

 The main symptom is warmth, tenderness, and redness on the skin.

 Treatment: Penicilline-V or Oxy-tetracycline 500 mg for 7-10 days. Erythema and edema with vesicle formation on the hand and fifth digit. Spirochetes Borelli Burgdorferi

 Lyme disease is a multisystem disorder with prominent skin findings that is caused by Borrelia species of spirochetes.

 Can occur at any time of the year but most cases present in the summer.

 If diagnosed in its early stages, it is a completely curable illness.

 The principle vector of BB infection is Ixodes tick (50% of the patients recall a tick bite).

All stages of the bite are capable of transmitting the disease but the nymphal stage feeding in early summer is the most common vector. Clinical Picture 3 stages: Stage 1:  ECM is present in up to 75% of the patients, after 3-30 day it appears at the site of the bite as an erythematous papule that gradually enlarges to an annular configuration with central cleaning.  ECM heals spontaneously within weeks to months.  Annular lesion may develop later in other parts of the body.  Urticaria, malar erythema perioral swelling may rarly occur.  Hp: superficial and deep perivascular & interstitial lymphohistocytic infiltrate containing plasma cells. Spirockittes can be recognized in 40 % of cases. Stage 2:

 Occurs between the 2nd and 7th months and involves mainly the nervus and CVS. - Neurological disorders: in 15% of patients e.g. meningetis, cranial N. palsies. - Heart diseases in 10 % of cases - Myalgia and arthralgia. - Lymphadenosis benigna cutis (LABC): Typical site is the areola and ear lobe. As an erythematous cyanotic asymptomatic nodules tend to grows for months then remain stationary for several years then disappear.

 HP: dense dermal infiltrate of lymphocytes, histocytes in a follicular pattern. Appendages and BV aren’t involved. Normal epidermis separated from dermal infiltrate by Grenz zone.

 Treatment: topical & IL steroids or penicillin. Stage 3:

 develop weeks to years after the onset of illness and involves:  Chronic arthritis in 60 % of cases (oligoarticular, affect large joints as knee and wrist).

 Neurologically: the manifestation of stage 2 become chronic. Acrodermatitis Chronica Atrophicans  ACA is a cutaneous manifestation of chronic Lyme disease.

 ACA occurs 6 months to 8 years after the initial infection, predominantly in women 40–70 years of age, and appears to be associated with long-term persistence of Borrelia organisms in the skin.

 It is a biphasic disorder consisting of an early, easily treatable, inflammatory stage and a late, treatment- resistant, atrophic stage.

ACA The acral skin is atrophic, shiny and wrinkled, with prominent superficial veins. Clinical Picture  Initially, erythematous to violaceous plaques and nodules develop on the acral portion of the extremities, often insidiously.

 The skin is frequently doughy and swollen.

 In the late stage, the skin has a glistening (―cigarette-paper‖) appearance with prominent blood vessels.

 Fibrous nodules may form on extensor surfaces (ulnar or tibial bands).

 Hypopigmentation, hyperpigmentation, pain, pruritus, hyperesthesia, paresthesias and scaling may also be present.

 Rarely, the condition may be complicated by the development of BCCs or SCCs.  In biopsy specimens of early lesions, a dermal perivascular lymphocytic infiltrate with plasma cells, telangiectatic endothelial-lined spaces, and mild epidermal atrophy is seen.

 Histologic examination of late lesions shows an atrophic epidermis and an interstitial lymphocytic infiltrate with plasma cells and occasional histiocytes and mast cells.

 The dermis may be attenuated, with periadnexal fibrosis. Bacteria previously classified as fungi Actinomycosis  Actinomycosis is a subacute or chronic bacterial infection characterized by suppurating + granulomatous inflammation + sinus formation.

 Actinomyces israelii, is the most common causative organism. It is part of the normal flora of the oral cavity, GIT and female genital tract.

 Men are affected 3 times more often than women.

 Humans are the only known reservoir for Actinomyces spp.

 The most important predisposing factor is trauma, especially dental procedures.

Clinical Picture  Cervicofacial actinomycosis (57% of patients ―lumpy jaw‖):  There is Initial bluish swelling in the mandibular area  progresses to brawny erythematous nodules,  The nodule gradually increase in size and form fistulous abscesses.  These drain purulent material with characteristic yellow ―sulfur granules‖ that represent clumps of bacteria.  Multiple sinus tracts, fever, pain and leukocytosis may develop. Lymphadenopathy is usually absent.

1ry cutenous type (uncommon) SC nodules on exposed skin with sinus and may be enlarged LN.

 Pulmonary actinomycosis (15–20% of patients).

 Occurs after bacteria gain access to the lung through the aspiration of infected oral material.  Pulmonary cavities are usually seen at the bases of the lungs.  Extension to the pleura and chest wall may occur, and pleurocutaneous fistulas can develop.

 Gastrointestinal actinomycosis (15% of patients).

 Preceded by trauma or inflammatory disease but may occur spontaneously.  Granulomatous lesions involving the bowel can eventually extend to the abdominal wall, producing a brawny, erythematous mass with draining sinus tracts. Cervicofacial actinomycosis or “lumpy jaw” Treatment

 The drug of choice is penicillin G or ampicillin:

 Deep seated infection treated for 2-6 weeks of IV therapy followed by oral penicillin for 3-12 months.  Acute infection: 2-3 weeks of oral penicillin + incision, draining and surgical incision of the sinus.

 Tetracycline, erythromycin, chloramphenicol have been tried.

Nocardiosis  is acute to chronic supperative disease caused by various species of A. Nocardia, a filamentous, Gram-positive, acid-fast organism.

 Clinically 3 major forms of 1ry cutenous nocardiosis: 1- Mycetoma 2- Lymphocutenous nocardiosis. 3- Superficial cutenous nocardiosis.

 Treatment 1- Sulfonamide drug of choice. 2- Minocycline. 3- Surgical treatment for SC abcesses.

Cutaneous Anthrax  It is caused by B. anthracis

 People get infected with anthrax when spores get into the body. the spores can be activated and become anthrax bacteria.

 The bacteria can multiply, spread out in the body, produce toxins, and cause severe illness.

 This can happen when people breathe in spores, eat food or drink water that is contaminated with spores, or get spores in a cut or scrape in the skin.

 Cutaneous anthrax is the most common form of anthrax infection, and it is also considered to be the least dangerous.

 Infection usually develops from 1 to 7 days after exposure.

 Without treatment, up to 20% of people with cutaneous anthrax may die.

 However, with proper treatment, almost all patients with cutaneous anthrax survive. Clinical Picture Clinical forms: cutaneous, pulmonary and gastrointestinal.

Cutaneous form: malignant pustule at the site of inoculation which spread and become hemorrhagic→ central eschar with surrounding non-pitting edema→ eschar slough→shallow ulceration. Treatment  Ciprofloxacin or doxycycline.  Rhinoscleroma is a slowly progressive, chronic granulomatous infection involving the nose and upper respiratory tract.

 Caused by Klebsiella rhinoscleromatis, a short, immotile Gram-negative bacillus that is a subspecies of K.pneumoniae.

 Deficiencies of cellular, but not humoral, immunity cause ineffective phagocytosis by macrophages, giving rise to large, vacuolated, non-lipidized histiocytes with intracellular bacteria (Mikulicz cells). Clinical Picture  Stage one: rhinitic/catarrhal/atrophic: • Non-specific rhinitis. • Purulent rhinorrhea and crusting. • Nasal obstruction.  Stage two: granulomatous/infiltrative/hypertrophic: • Granulomatous nodules form in the nose, pharynx and larynx. • Dysphonia, anosmia and anesthesia of soft palate may occur. • Epistaxis, deformity of the nose, destruction of the nasal cartilage (Hebra nose).  Stage three: sclerotic/cicatricial: • Nodules replaced by fibrous tissues with resultant extensive scarring and stenosis often requiring surgical intervention (e.g. tracheotomy, reconstruction of the airway).

Treatment  Antimicrobial therapy for 6 months or until nasal biopsy is negative;

 Tetracycline is first-line therapy along with surgical correction of obstructed airway.  Rifampin and ciprofloxacin are alternative antibiotics.  Sclerotic lesions respond to ciprofloxacin.  Bacterial superinfection is common, requiring treatment with clindamycin or a third-generation cephalosporin.  Pseudomonas aeruginosa is a ubiquitous Gram-negative, strictly aerobic, motile bacillus.

 It is widely distributed in the soil and on plants, growing especially well in aqueous environments.

 This organism has relatively low virulence and usually requires a local anatomic or immunologic defect to cause disease.  Primary cutaneous infection with P. aeruginosa can occur in healthy individuals in areas exposed to high levels of moisture in conjunction with skin barrier disruption; these infections have a very good prognosis.

 In contrast, cutaneous manifestations of Pseudomonas sepsis in immunocompromised individuals are associated with a grave prognosis. Superficial infection of the skin with Pseudomonas. There is maceration, erosions and moth-eaten appearance of the skin. Green Nail Syndrome  The nail develops green–black to green–blue discoloration due to pyocyanin, a blue–green pigment produced by P. aeruginosa.

 Predisposing factors include frequent or prolonged exposure to water, excessive use of detergents and soaps, nail trauma, and other causes of onycholysis.

 Treatment  Avoidance of predisposing factors.  Clipping the nail.  Topical application of a quinolone or aminoglycoside solution for 1–4 months.  In refractory cases, removal of the affected nail can be considered. Common Diagnostic Tests

 Biopsy.  Patch Testing: Allergy test.  Tzanck smear: detect type of cells in chicken pox, H. simplex, H. zoster, bullous diseases.  Skin scrapings.  Culture and sensitivity.  Diascopy: visualization by special microscope  Wood’s light examination: Use of U.V. rays Prevention and control of Bacterial skin diseases  Personal hygiene is the most effective methods for prevention and control of bacterial infections.

 The following points illustrate the possible preventive methods for bacterial skin infections:  Washing of hands with warm water and soap before touching broken skin.  Washing the body with warm water and soap preferably everyday to remove dust and dirt.  Wearing the right size and type of clothes to suit local weather conditions.  After washing clothes, if possible, iron it before wearing.  Regular exposure of the skin to air and sunlight is beneficial.