14-Bacterial%20Infections.pdf

Bacterial skin infections By Salsabiela Bani Hamad Introduction: Intact skin forms a highly effective barrier against invading pathogenic bacteria. Many micro-organisms come into contact with the skin and some live there as part of the normal skin flora, but they rarely cause disease. Normal skin fl...

Bacterial skin infections By Salsabiela Bani Hamad Introduction: Intact skin forms a highly effective barrier against invading pathogenic bacteria. Many micro-organisms come into contact with the skin and some live there as part of the normal skin flora, but they rarely cause disease. Normal skin flora consists of:  Coagulase-negative Staphylococcus, Corynebacterium, Diphtheroids, and 𝛼-haemolytic Streptococci in the epidermis.  Propioni- bacterium in the pilosebaceous unit. Coachi Normal flora competes with invading pathogenic micro-organisms, thereby acting as a ‘biological shield’. However, if the host immune system weakens or there is a change in the micro-environment (such as an underlying skin disease) this may allow such bacteria to become pathogenic. DM Introduction: Bacterial skin infections may be acquired from the external environment (from plants, soil, fomites, animals, or other humans) by implantation, direct contact, aerosols, or water-borne transmission. Patients with a bacterial skin infection may recall an episode of trauma to the skin or they may have a history of ongoing skin disease. A more detailed history may reveal contact with potentially contaminated water via bathing, animal contact, travel abroad or other family members/close contacts similarly affected. However, many patients will not have any obvious source from history taking alone. Clinical presentation: Acute bacterial infections in the skin generally produce some or all of the classical characteristics of acute inflammation: erythema, swelling/edema, heat/warmth, To and pain/discomfort. Cardinalsion Patients may develop systemic symptoms such as fever and malaise. watarea Investigations: 1. Bacterial swabs: For microscopy and culture Microbiological testing can identify1bacterial species, 2antibiotic resistance/sensitivity patterns, and bacterial toxin production. Lesional skin and carrier sites can be swabbed. 2. Nasal swabs: May identify Staphylococcus aureus carriers (MRSA) who can suffer from recurrent infections because of bacterial shedding from the nose. mygmersa indication ((When taking swabs they should be moistened in the transport media before contact with the skin and each surface of the swab should be rotated on the infected skin surface)). directly Dry 0 needto be misted Investigations: 3. Panton-Valentine Leukocidin (PVL): Is a toxin produced by some strains of S. aureus which cause the bacteria to be highly virulent and highly transmissible. PVL-positive S. aureus often presents with multiple/recurrent boils not improving with short courses of antibiotics. tetandstainauretrosuse PVL toxin 4. In severe skin infections or when you suspect mycobacterial infections, take a skin biopsy for culture and polymerase chain reaction (PCR). Multiple abscesses (due to PVL staphylococcus aureus infection Treatment: at 1. Antiseptics: Skin washes or creams containing chlorhexidine hydrochloride can be helpful in removing superficial bacteria. Potassium permanganate soaks or diluted bleach can be very effective at treating any cutaneous infections, particularly on the lower legs. 2. Topical antibiotics: Applied twice daily For mild localized infections. Fusidic acid, mupirocin, neomycin, polymyxins, retapamulin, silver sulphadiazine, and metronidazole are all available in topical formulations. S/E: Prolonged exposure to topical antibiotics leads to the selection of resistant organisms and rarely contact dermatitis (esp neomycin) 3. Systemic antibiotics: For more extensive cutaneous bacterial infections. Treatment:  For Staphylococcal: Is provided by flucloxacillin, erythromycin, clarithromycin, azithromycin, cofluampicil (contains flucloxacillin and ampicillin), co-amoxiclav, clindamycin, fusidic acid, ciprofloxacin, cefuroxime, dicloxacillin, cloxacillin, linezolid, pristinamycin, and roxithromycin.  For MRSA: Use vancomycin, nafcillin, daptomycin, or tigecycline.  For Streptococcal: Is provided by penicillin V, amoxicillin, flucloxacillin, erythromycin, clarithromycin, azithromycin, co- amoxiclav, cefuroxime, ceftazidime, clindamycin, pristinamycin, roxithromycin, vancomycin and levofloxacin. I Bacterial Skin Infections: Superficial Bacterial Infections: - Impetigo (staph, strep) Bacterial folliculitis (staph) Boils (Abscesses) (staph) Pseudofolliculitis not Bacteria Erythrasma (cprynobcterium) Deeper Bacterial Infections: - Erysipelas (strep) Cellulitis (strep) Necrotizing Fasciitis (Mixed aerobic and anaerobic) Staphylococcus Scalded Skin Syndrome (staph) Ecthyma (strep) Mycobacterial disease Other Infections R Superficial Bacterial Infections: Superficial infections: Golden crust Impetigo: Is usually caused by S. aureus or Streptococcus pyogenes. Is highly contagious between close contacts. develops rapidly into clusters of pustules and vesicles which break down into the classic golden crusts. Two types: Non-Bullous & Bullous. t staph Vasicula and Pustial t most10 staph seeme strep t nostrep Impetigo: whay only staph Bullous lesions are more likely to occur with Staphylococcal or infections which produce epidermolytic toxins A/B. g p Streptococcus is more likely to be the causative organism if there is associated regional lymphadenopathy. Jaap nonbullas Several family members may be affected simultaneously, particularly in conditions of poor hygiene in hot humid climates. There may be an association with minor trauma such as insect bites. me Secondary impetigo may co-exist with any pre-existing skin lesion. Treatment: - Topical treatment includes antiseptic washes, fusidic acid, mupirocin, and polymyxins. - Oral antibiotics most frequently used include flucloxacillin and erythromycin. Bacterial folliculitis Defined as an infection in the hair follicles which may be superficial and/or deep and is usually caused by S. aureus. 2 Are frequently mild and self-limiting. Clinically, there is a pustule and erythema around the follicular orifice. Folliculitis may result from minor trauma such as hair removal by shaving or waxing. multiblearthamaspapal andpustule Deeper follicular infections are characterized by abscess formation, min boils, and furunculosis. man my When several furuncles coalesce they form a carbuncle. Inflammation ofHair andsurrounding follicle tissa Hot-tub folliculitis: - Caused by Pseudomonas aeruginosa. - Appears within 2 days of exposure to contaminated water or water accessories (such as wet suits). Lemitted by self comprmizes immune Pseudofolliculitis: Has similar clinical appearance to bacterial folliculitis but this is caused by occlusion of the follicular openings by heavy emollients rather than bacterial infection. Lesions are all at the same stage of development and are clinically very monomorphic, and the pustules are sterile. monetarist Pond Acne CopDX Pseudofolliculitis barbae: In the beard area. Coarse curly hair punctures the skin adjacent to the hair follicle resulting in a foreign body reaction with inflammation which can become chronic and lead to scarring. In the occipital area of the scalp acne keloidalis nuchae results from folliculitis and perifolliculitis with resultant alopecia and keloid scarring from chronic inflammation. Aalmost exclusively in black males who shave their hair very short. Erythrasma: Usually affects the flexural skin sites, particularly the axilla and groin. There is superficial scaling and mild inflammation, often with a reddish-brown discoloration. Causative bacterium Corynebacterium minutissimum from skin scraping can be useful for dx. Under Wood’s ultraviolet light the affected skin fluoresces pink. First-line treatment is usually oral erythromycin (250 mg QDS for 7–14 days), but if topical treatment is preferred, then clotrimazole, miconazole, fusidic acid, or neomycin can be effective. Deeper Bacterial Infections: Erysipelas: Caused by a Streptococcus infection Over approximately 48 h the inflammation spreads across the skin with a characteristic red, shiny, raised, spreading plaque with a well-demarcated edge. Occasionally, blistering may occur at the active edge; patients may have fever and malaise. The face and lower legs are most frequently affected Differential diagnosis of erysipelas on the face includes contact dermatitis, photodermatitis, rosacea, systemic lupus erythematosus, and fifth disease ‘slapped cheek’ Erysipelas: If the infection is severe, treat with: - Intravenous benzylpenicillin - Orally with amoxicillin, roxithromycin, or pristinamycin for 1–2 weeks. Recurrent attacks are reported in 20% of patients with predisposing conditions; these individuals may require long-term secondary prophylaxis (Penicillin V 500 mg daily). Erysipelas: Erysipelas is the local manifestation of a group A Streptococcal infection; however, the same organism through the production of toxins or superantigens can cause other skin lesions such as: (a) Scarlet fever. (b) Erythema nodosum. (c) Guttate psoriasis. (d) Acute generalized vasculitis. In Erysipelas the Streptococcus organisms invade the dermis and penetrate the lymphatics, which clinically is well demarcated; this contrasts with the clinical appearance of cellulitis (infection in the deeper layers), which is poorly demarcated. Cellulitis: Develops more slowly than erysipelas and has a poorly defined margin and marked regional lymphadenopathy. Patients may have a fever and general malaise. S. pyogenes (also groups C/G 𝛽-haemolytic Streptococcus, or rarely S. aureus) organisms invade deeper tissues than those found in erysipelas. The lower leg is the most common site affected. Patients may have underlying dermatoses such as a diabetic foot ulcer, tinea pedis, or stasis dermatitis which act as a portal of entry for the bacteria In severe infections intravenous IV benzylpenicillin may be needed for up to a week as the infection settles slowly. Necrotizing fasciitis: Characterized by dusky purplish erythema associated with extensive life-threatening necrosis of the deeper tissue because of rapidly progressive mixed (anaerobic and aerobic bacteria) infection of the deep fascia leading to gas formation in the subcutaneous tissues. Patients often have a history of recent trauma or surgery. There is usually severe pain initially at the site followed by anaesthesia. Necrotizing fasciitis: Dusky erythema associated with necrosis at the skin surface is usually the tip of the iceberg with much more extensive lifethreatening necrosis of the deeper tissues. Treatment: Urgent surgical debridement and broad-spectrum antibiotics are indicated. Staphylococcus scalded skin syndrome (SSSS): Caused by strains of S. aureus that produce exfoliative toxins A/B resulting in intraepidermal splitting (the target is desmoglein 1 which is responsible for keratinocyte adhesion). A localized form of the disease is called bullous impetigo. The clinical presentation in children below 5 years of age is usually with conjunctivitis, otitis media or a nasopharyngeal infection, with fever, malaise, and red tender skin. Generalized cutaneous erythema is followed by >> widespread superficial blistering (Nikolsky sign positive) and exfoliation which may be most striking in the flexures. Staphylococcus scalded skin syndrome (SSSS): Although most children are not unwell there is a 4% mortality rate for generalized SSSS. Treatment: - Give systemic antibiotics to treat Staphylococcus. - If patients fail to respond, then consider treating for MRSA which has a higher mortality rate. Ecthyma: Is often referred to as a deeper form of impetigo as the group A𝛽-hemolytic Streptococci (S. pyogenes) invade the dermis leading to superficial ulcers. Lesions start as small pustules that have adherent crust and underlying ulceration Most commonly occur on the lower legs of children and elderly people who live in humid climates. Lesions usually heal slowly with scarring Mycobacterium infections Mycobacterium infections Clinical manifestations of mycobacterial infections are largely determined by the ability of the host to mount an immune response. Cutaneous M. tuberculosis (TB) is rare even in endemic areas. TB in the skin usually occurs as a secondary manifestation of disease with its primary focus in the respiratory tract. The most common manifestation is lupus vulgaris which usually presents on the head and neck. Lesions appear as slowly growing well-demarcated red-brown papules that coalesce to form indolent plaques of a gelatinous nature: the so-called ‘apple-jelly nodules’. Mycobacterium infections: Allergic-type hypersensitivity reactions called tuberculids can occur in the skin of patients with underlying TB. Tuberculids are thought to represent hypersensitivity reactions to antigenic fragments of dead bacilli deposited in the skin via hematogenous spread. Tuberculids include erythema induratum (Bazin’s disease) where patients present with tender nodules and plaques that ulcerate and heal with scarring on the lower legs. Atypical Mycobacteria infections: Atypical mycobacteria (ATM) are usually found in the environment in vegetation and water 1- Mycobacterium marinum: or ‘fish tank’ or ‘swimming pool granuloma’ usually occurs because of contact with infected tropical fish or contaminated water. The hand or fingers are most frequently affected; initially, a single warty nodular and occasionally pustular lesion appears with subsequent sporotricoid spread along local lymphatics, forming a chain of nodules. 2- Mycobacterium ulcerans: causes extensive non-painful ulceration usually on the limbs in children/young adults living in tropical humid areas associated with minor skin trauma and contact with the mycobacterium in standing water. Other Infections Syphilis: Is caused by the spirochete bacterium Treponema pallidum which is transmitted through sexual intercourse, transplacental spread, and via unscreened blood transfusions. The incidence of syphilis is steadily increasing due to co-infection with human immunodeficiency virus (HIV). Serology is needed to know whether patients have a previous or current infection, which will subsequently guide management and contact tracing. Syphilis: Primary syphilis manifests as a painless genital ulcer at the site of inoculation. Cutaneous manifestations of secondary syphilis are characterized by a widespread eruption of red-brown scaly patches and macules that affects the trunk and limbs (particularly palms and soles). Rocky Mountain spotted fever (RMSF): One of the most common rickettsial infections (Rickettsia rickettsii) in the USA and has a 4% mortality rate. The most common vector of RMSF is the dog tick. Within a week of the bite >> patients present with high fever, headache, myalgia, and a petechial rash which characteristically appears on the palms and soles but may spread to the trunk. There may be a necrotic lesion at the site of the tick bite. Treat adults with doxycycline 100mg twice daily for approximately 1 week and children with azithromycin for 5 days. Bacillary angiomatosis: Caused by Bartonella henselae and Bartonella quintana infections. Clinical manifestations are most commonly seen in the skin and mucous membranes, but the underlying visceral disease (especially liver) may occur simultaneously. Patients usually present with multiple small cherry-like haemangiomas on the skin which appear over weeks to months. Present in HIV patients with multiple small haemangioma-like papules. Serology rather than culture is usually used to confirm the diagnosis (indirect fluorescent assay or ELISA IgG >1:64 indicates likely current infection). Erythromycin 500 mg qds for up to 12 weeks is recommended, or 4−6 weeks of azithromycin 500 mg daily. Cat-scratch disease : Is caused by the bacterium B. henselae. Crusted nodules appear within 3–12 days at the site of a scratch (usually by a kitten) associated with the development of regional painful lymphadenopathy 1 or 2 months later. The disease usually undergoes spontaneous remission within 2–4 months. A 5-day course of azithromycin can speed up recovery. Thank You