BACTERIAL SKIN INFECTION
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: impetigo, ecthyma, folliculitis, furunculosis, carbuncle, sycosis.
2. Secondary infection: eczema, infestations, ulcers, …etc.
3. Effect of bacterial toxin: staph.-associated scalded skin syndrome (SSSS), toxic shock syndrome. Streptococcal Infection (gp A streptococci)
1. Direct inf. of skin or subcut. tissue: Impetigo, ecthyma, cellulitis, vulvovaginitis, perianal inf., ulcers, blistering, necrotizing fasciitis.
2. 2ry inf.: eczema, infestations, ulcers, …etc. Tissue damage from circulating toxin: scarlet fever, 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-bullous impetigo: 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 pathogenic bacteria. 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 ―boils‖ 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/Carbuncles Frunculosis/Boil It is a staphylococcal infection 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 Erysipelas 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.
Lymphadenopathy are frequent.
Complications: Recurrences may lead to lymphedema. Subcutaneous abscess. 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 pimples‖). 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 gangrene).
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. Erysipeloid 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
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 abscesses + 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 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 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 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.