Bacterial Skin Infections PDF

Bacterial Skin Infections Omar Younis Abdullah MSc / St. Johns Institute of Dermatology / KCL, London, UK. Member of the British Association of Dermatologists (BAD) Lecture’s Objectives To know about very...

Bacterial Skin Infections Omar Younis Abdullah MSc / St. Johns Institute of Dermatology / KCL, London, UK. Member of the British Association of Dermatologists (BAD) Lecture’s Objectives To know about very important skin infections (Bacterial Infections) To get the information on how to diagnose them To understand how these diseases behave and their complications and prognosis To obtain the necessary knowledge on how to treat them Impetigo 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 and nonbullous impetigo. Both begin as vesicles with a very thin, fragile roof consisting only of stratum corneum. S. aureus is now known to be the primary pathogen in both bullous and nonbullous impetigo. Children in close physical contact with each other have a higher rate of infection than do adults. Impetigo may occur after a minor skin injury such as an insect bite, but it most frequently develops on apparently unimpaired skin. Glomerulonephritis following streptococcal infection may be a complication of impetigo caused by certain strains of Streptococcus pyogenes. Bullous Impetigo Bullous impetigo (staphylococcal impetigo) is caused by an epidermolytic toxin produced at the site of infection and usually is not secondarily contaminated by streptococci. The toxin causes intraepidermal cleavage below or within the stratum granulosum. Bullous impetigo is most common in infants and children but may occur in adults. It typically occurs on the face, but it may infect any body surface. There may be a few lesions localized in one area, or the lesions may be so numerous and widely scattered.  The center of the thin-roofed bulla collapses, but the peripheral area may retain fluid for many days in an inner tube–shaped rim. A thin, flat, honey-colored, “varnishlike” crust may appear in the center and, if removed, discloses a bright red, inflamed, moist base that oozes serum. In most cases, a tinea-like scaling border replaces the fluid-filled rim. Nonbullous Impetigo Nonbullous impetigo originates as a small vesicle or pustule that ruptures to expose a red, moist base. A honey-yellow to white-brown, firmly adherent crust accumulates as the lesion extends radially. The skin around the nose and mouth and the limbs are the sites most commonly affected. Most lesions heal without scarring.  A pure culture of group A beta-hemolytic streptococci may sometimes be isolated from early lesions, but most lesions promptly become contaminated with staphylococci. Regional lymphadenopathy is common (unlike bullous impetigo). The antistreptolysin O (ASO) titer does not increase to a significant level following impetigo. Antideoxyribonuclease B (anti-DNase B) increases to high levels and is a much more sensitive indicator of streptococcal impetigo. Prevention of Impetigo Mupirocin (Bactroban) applied three times daily to sites of minor skin trauma (e.g., mosquito bites and abrasions) can be efficacious as a preventive treatment. Recurrent Impetigo Patients with recurrent impetigo should be evaluated for carriage of S. aureus. The nares are the most common sites of carriage, but the perineum, axillae, and toe webs may also be colonized. Mupirocin ointment or cream (Bactroban) applied to the nares and the above sites twice each day for 5 days significantly reduces S. aureus carriage. Treatment of Impetigo Impetigo may resolve spontaneously or become chronic and widespread; 2% mupirocin ointment or cream is effective. Also retapamulin and fucidic acid creams/ointments. Oral antibiotics should be considered for patients with impetigo who have extensive disease or systemic symptoms. A 5- to 10-day course of oral antibiotics induces rapid healing. Start cephalexin in non–penicillin- allergic patients. Cellulitis and Erysipelas Cellulitis and erysipelas are skin infections characterized by erythema, edema, and pain. In most instances there is fever and leukocytosis. Both may be accompanied by lymphangitis and lymphadenitis. Pathogens enter at sites of local trauma or abrasions and at psoriatic, eczematous, or tineal lesions. Erysipelas involves the superficial layers of the skin and cutaneous lymphatics; cellulitis extends into the subcutaneous tissues. Cellulitis is an infection of the dermis and subcutaneous tissue that is usually caused (together with erysipelas) by a group A streptococcus / S. aureus in adults and Haemophilus influenzae type B in children younger than 3 years of age. Cellulitis typically occurs near surgical wounds or a cutaneous ulcer or, like erysipelas, may develop in apparently normal skin. There is no clear distinction between infected and uninfected skin. Recurrent episodes of cellulitis occur with local anatomic venous or lymphatic abnormalities (surgery, radiation).  Erysipelas is an acute, inflammatory form of cellulitis that differs from other types of cellulitis in that lymphatic involvement (“streaking”) is prominent. The area of inflammation is raised above the surrounding skin, and there is a distinct demarcation between involved and normal skin. The lower legs, face, and ears are most frequently involved. Treatment of cellulitis and erysipelas: Treatment of uncomplicated cellulitis: Oral β- lactam antibiotics, clindamycin, TMP-SMX, linezolid, doxycycline). In hospitalized patients with complicated skin and soft tissue infection (cSSTI) which is defined as patients with deeper soft tissue infections, surgical/traumatic wound infection, major abscesses, infected ulcers and burns), in addition to surgical debridement: Intravenous vancomycin, linezolid or clindamycin. Also … Elevation of the affected area promotes drainage of the edema and hastens recovery for lower leg infections. Pain can be relieved with cool compresses and analgesics. Treat underlying conditions that may predispose to the infection, such as tinea pedis, stasis dermatitis, or trauma. FOLLICULITIS Folliculitis is inflammation of the hair follicle caused by infection, chemical irritation, or physical injury. Inflammation may be superficial or deep in the hair follicle. Folliculitis is very common and is seen as a component of a variety of inflammatory skin diseases. Staphylococcal Folliculitis Staphylococcal folliculitis is the most common form of infectious folliculitis. One pustule or a group of pustules may appear on any part of the body (hair-bearing parts only), usually without fever or other systemic symptoms. May occur because of injury, abrasion (as in shaving), or nearby surgical wounds or draining abscesses. It may also be a complication of occlusive topical steroid therapy. The inflammation is superficial (confined to the upper part of the hair follicle). Clinically, it is manifested as a painless (sometimes pruritic or tender) pustule that eventually heals without scarring. Rx: Topical +/- oral antibiotics are used in most cases. Pseudofolliculitis Barbae (Razor Bumps) Pseudofolliculitis barbae (PFB) is a foreign-body reaction to hair. Clinically, there is less inflammation than with staphylococcal folliculitis. The condition occurs on the cheeks and more commonly the neck in individuals who are genetically inclined to have tightly curled, spiral hair, which can become ingrown (usually blacks). If cut below the surface by shaving, the sharp-tipped whisker may curve into the follicular wall or emerge and curve back to penetrate the skin. A tender/pruritic red papule or pustule occurs at the point of entry and remains until the hair is removed. Pseudofolliculitis can occur also in the axillae, pubic area, and legs. Pseudofolliculitis of the beard is a significant problem in the armed services and in professions in which individuals are required to shave regularly and very closely. Furuncles and carbuncles A furuncle (also called abscess or boil) is a walled-off collection of pus that is a painful and tender, firm or fluctuant mass, originating from a single infected hair follicle. An abscess is a cavity formed by finger-like loculations of granulation tissue and pus that extends outward along planes of least resistance. Age: furuncles increase in frequency after puberty. Furunculosis occurs as a self-limited infection in which one or several lesions are present or as a chronic, recurrent disease that lasts for months or years, affecting one or several family members. Most patients with sporadic or recurrent furunculosis appear to be otherwise healthy and have an intact immune system.  Lesions may occur at any site but favor areas prone to friction or minor trauma, such as underneath a belt, the anterior thighs, buttocks, groin, axillae, and waist. S. aureus is the most common pathogen. Other organisms, either aerobic (E. coli, P. aeruginosa, Enterococcus faecalis) or anaerobic (Bacteroides, Lactobacillus, Peptococcus, Peptostreptococcus), may cause furuncles. In general, the microbiology of abscesses reflects the microflora of the anatomic part of the body involved. Anaerobes are found in perineal abscesses for example. The lesion begins as a deep, tender, firm, red papule that enlarges rapidly and then becomes fluctuant. The patient may sometimes have a fever or systemic symptoms. Pain becomes moderate to severe as purulent material accumulates. Pain is most intense in areas where expansion is restricted, such as the neck and external auditory canal. Events: The abscess either remains deep and reabsorbs or points and ruptures through the surface. The abscess cavity contains a surprisingly large quantity of pus and white chunks of necrotic tissue. The point of rupture heals with scarring.  Carbuncles are aggregates of infected 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. 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 (V.S. furuncles). In the preantibiotic era, there were some fatalities. Treatment of Furuncles and Carbuncles: Many furuncles are self-limited and respond well to frequent applications of a moist, warm compress, which provide comfort and probably encourage localization and pointing of the abscess. Incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate. Antistaphylococcal antibiotics (topical and systemic) for 5 to 10 days. Necrotizing Skin and Soft Tissue Infections Necrotizing skin and soft tissue infections are often deep and devastating. They may involve the fascial and/or muscle compartments and can cause destruction of tissue and be fatal. They are often secondary infections that develop from a break in the skin from trauma or surgery. They are usually caused by streptococci or mixed bacterial flora. Necrotizing Fasciitis Necrotizing fasciitis (NF) is an infection of the subcutaneous tissue that results in the destruction of fascia and fat. The infection is most frequently polymicrobial. Ten percent of infections are caused by group A streptococcus and can lead to toxic shock. NF most frequently occurs in the extremities, with a predilection for the lower leg. NF may mimic deep vein thrombosis.  Predisposing factors include: trauma (often trivial), burns, splinters, surgery, childbirth, diabetes mellitus, varicella, immunosuppression, renal failure, arteriosclerosis, odontogenic infection, malignancy, and alcoholism. Nonsteroidal antiinflammatory agents may alter the immune response, causing a minor infection to become fulminant. Extension from a skin lesion occurs in 80% of cases. The initial lesion is often trivial, such as a minor abrasion, insect bite, injection site (drug addicts), or boil; 20% of patients have no visible skin lesion. Initially there is pain, erythema, edema, cellulitis, and high fever. The patient may be disoriented and lethargic. The local site shows cellulitis (90% of cases), edema (80%), skin discoloration or gangrene (70%), and anesthesia of involved skin. A wooden-hard feel of the subcutaneous tissues is characteristic.  Many patients are diagnosed with cellulitis and sent home; they return when the condition worsens. The most consistent clinical clue is unrelenting pain out of proportion to the physical findings even if there is only mild or no fever or erythema. Typically there is diffuse swelling of an arm or leg and intense pain on palpation. About 1 or 2 days after symptom onset, the patient has high fever, leukocytosis, edema with central patches of dusky blue discoloration, weeping blisters, and borders with cellulitis.  Bullae with clear fluid rapidly turn violaceous. Septicemia may develop secondarily and should be strongly suspected in the presence of fever, anorexia, nausea, diarrhea, confusion, and hypotension. Progression to gangrene, sometimes with myonecrosis, and an extension of the inflammatory process along fascial planes are possible. Twenty-five percent will die of septic shock and organ failure. Bacteria Monomicrobial Form: S. pyogenes, S. aureus, Vibrio vulnificus, Aeromonas hydrophila, and anaerobic streptococci (e.g., Peptostreptococcus species) are most often isolated. Staphylococci and hemolytic streptococci can occur simultaneously. S. pyogenes are most often seen after varicella or minor scratches and insect bites. Mortality in this group approaches 50% to 70% in patients with hypotension and organ failure. Polymicrobial Form: Most organisms originate from the bowel flora (e.g., coliforms and anaerobic bacteria). The polymicrobial necrotizing infection is associated with:(1) surgical procedures involving the bowel or penetrating abdominal trauma, (2) decubitus ulcers or perianal abscesses, (3) sites of injection in injection drug users, and (4) extension from a Bartholin abscess or a minor vulvovaginal infection. References Johnson MK. Impetigo. Adv Emerg Nurs J. 2020 Oct/Dec;42(4):262-269. Lin HS, Lin PT, Tsai YS, Wang SH, Chi CC. Interventions for bacterial folliculitis and boils (furuncles and carbuncles). Cochrane Database Syst Rev. 2021 Feb 26;2(2):CD013099. Stevens DL, Bryant AE. Streptococcus pyogenes Impetigo, Erysipelas, and Cellulitis. 2022 Sep 7 [updated 2022 Oct 4]. In: Ferretti JJ, Stevens DL, Fischetti VA, editors. Streptococcus pyogenes: Basic Biology to Clinical Manifestations [Internet]. 2nd ed. Oklahoma City (OK): University of Oklahoma Health Sciences Center; 2022 Oct 8. Chapter 23. PMID: 36479753. Patel TS, Dalia Y. Pseudofolliculitis Barbae. JAMA Dermatol. 2022 Jun 1;158(6):708. Chen LL, Fasolka B, Treacy C. Necrotizing fasciitis: A comprehensive review. Nursing. 2020 Sep;50(9):34-40. thank you