BACTERIAL and VIRAL SKIN AND SOFT TISSUE INFECTIONS Meral SÖNMEZOĞLU, MD Yeditepe University Hospital Professor of Department of Infectious Diseases and Microbiology

Structure and Function of the Skin Learning Objective Describe the structure of the skin and mucous membranes and the ways pathogens can invade the skin.

The Structure of Human Skin Perspiration and sebum contain nutrients Salt inhibits microbes Lysozyme hydrolyzes peptidoglycan Fatty acids inhibit some pathogens Figure 21.1

Mucous Membranes Line body cavities The epithelial cells are attached to an extracellular matrix Cells secrete mucus Often acidic Some cells have cilia In eyes, washed by tears with lysozyme

Normal Microbiota of the Skin Learning Objective Provide examples of normal skin microbiota, and state the general locations and ecological roles of its members.

Normal Microbiota of the Skin Gram-positive, salt-tolerant bacteria Staphylococci Micrococci Diphtheroids Figure 14.1a

Normal Microbiota of the Skin Grow on oils Aerobes on surface Corynebacterium xerosis Anaerobes in hair follicles Propionibacterium acnes Yeast Malassezia furfur

Microbial Diseases of the Skin Exanthem: Skin rash arising from another focus of the infection Enanthem: Mucous membrane rash arising from another focus of the infection

Skin Lesions Figure 21.2

Bacterial Diseases of the Skin Learning Objectives Differentiate staphylococci from streptococci, and name several skin infections caused by each. List the causative agent, mode of transmission, and clinical symptoms of Pseudomonas dermatitis, otitis externa, acne, and Buruli ulcer.

Staphylococcal Skin Infections Staphylococcus epidermidis Gram-positive cocci, coagulase-negative Staphylococcus aureus Gram-positive cocci, coagulase-positive Clinical Focus, p. 593

Staphylococcus aureus Antibiotic resistant Leukocidin Resists opsonization Survives in phagolysosome Lysozyme resistant Exfoliative toxin Superantigen Clinical Focus, p. 593

Staphylococcal Biofilms Figure 21.3

Skin and Soft Tissue Infections Cellulitis Impetigo Erysipelas Abscess Animal bite Human bite Surgical site infection Necrotizing fasciitis

Purulent skin and soft tissue infections (SSTIs). Purulent skin and soft tissue infections (SSTIs). Mild infection: for purulent SSTI, incision and drainage is indicated. Moderate infection: patients with purulent infection with systemic signs of infection. Severe infection: patients who have failed incision and drainage plus oral antibiotics or those with systemic signs of infection such as temperature >38°C, tachycardia (heart rate >90 beats per minute), tachypnea (respiratory rate >24 breaths per minute) or abnormal white blood cell count (<12 000 or <400 cells/µL), or immunocompromised patients. Nonpurulent SSTIs. Mild infection: typical cellulitis/erysipelas with no focus of purulence. Moderate infection: typical cellulitis/erysipelas with systemic signs of infection. Severe infection: patients who have failed oral antibiotic treatment or those with systemic signs of infection (as defined above under purulent infection), or those who are immunocompromised, or those with clinical signs of deeper infection such as bullae, skin sloughing, hypotension, or evidence of organ dysfunction. Two newer agents, tedizolid and dalbavancin, are also effective agents in SSTIs, including those caused by methicillin-resistant Staphylococcus aureus, and may be approved for this indication by June 2014. Abbreviations: C & S, culture and sensitivity; I & D, incision and drainage; MRSA, methicillin-resistant Staphylococcus aureus; MSSA, methicillin-susceptible Staphylococcus aureus; Rx, treatment; TMP/SMX, trimethoprim-sulfamethoxazole. Dennis L. Stevens et al. Clin Infect Dis. 2014;cid.ciu296 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Staphylococcal Skin Infections Folliculitis: Infections of the hair follicles Sty: Folliculitis of an eyelash Furuncle: Abscess; pus surrounded by inflamed tissue Carbuncle: Inflammation of tissue under the skin Impetigo: crusting (nonbullous) sores, spread by autoinoculation

Nonbullous Lesions of Impetigo Figure 21.4

Scalded Skin Syndrome Toxic shock syndrome (TSS) Scalded skin syndrome Toxic shock syndrome toxin 1 Scalded skin syndrome Bullous impetigo Impetigo of the newborn

Lesions of Skin Syndrome Figure 21.5

Streptococcal Skin Infections Streptococcus pyogenes Group A beta-hemolytic streptococci Hemolysins Hyaluronidase Streptolysins M proteins

Group A Beta-Hemolytic Streptococci Figure 21.6

Ecthyma Presentation: Vesicle/pustule which enlarges over several days and becomes thickly crusted. When crust is removed a superficial saucer shaped ulcer remains with elevated edges. Nearly always on shins or dorsal feet. Heals in a few weeks with scarring. Agent: Staph or Strep. Heal with scaring Gangrene in predisposed individuals. Treatment: Clean, topical and systemic ABX.

Ecthyma

Scarlet Fever Presentation: 24 –48 hrs after Strep. Pharyngitis onset. Cutaneous: Widespread erythema with 1-2 mm papules. Begins on neck and spreads to trunk then extremities. Pastia’s lines – accentuation over skin folds with petechia. Circumoral pallor Desquamation of palms and soles at appox two wks. May be only evidence of disease. Other: strawberry tongue Causes: erythrogenic exotoxin of group A Strep. Culture to recover organism or use streptolysin O titer if testing is late. TX: PCN, E-mycin, Cloxacillin.

Scarlet Fever

Streptococcal Skin Infections Necrotizing fasciitis Erysipelas Figure 21.7

Necrotizing Fasciitis Presentation: Following surgery or trauma (24 to 48 hours) - erythema, pain and edema which quickly progress to central patches of dusky blue discoloration. Anesthesia of the involved skin is very characteristic. By day 4-5 the involved area becomes gangrenous. Infection of the fascia. Many causative agents. Aerobic and anaerobic cultures should be taken. Treatment: Early debridement. ABX. 20% mortality in best cases Poor prognostic factors: Age >50, DM, Atherosclerosis, involvement of trunk, delay of surgery >7 days.

Necrotizing fasciitis Necrotizing fasciitis is a rapidly progressive inflammatory infection of the fascia, with secondary necrosis of the subcutaneous tissues. The speed of spread is directly proportional to the thickness of the subcutaneous layer. Moves along the fascial plane. Has also been referred to as hemolytic streptococcal gangrene, Meleney ulcer, acute dermal gangrene, hospital gangrene, suppurative fasciitis, and synergistic necrotizing cellulitis. Fournier gangrene is a form of necrotizing fasciitis that is localized to the scrotum and perineal area.

Necrotizing fasciitis Necrotizing fasciitis may occur as a complication of a variety of surgical procedures or medical conditions, including cardiac catheterization, vein sclerotherapy, and diagnostic laparoscopy, among others . It may also be idiopathic, as in scrotal or penile necrotizing fasciitis. The causative bacteria may be aerobic, anaerobic, or mixed flora.

Necrotizing fasciitis The frequency of necrotizing fasciitis has been on the rise because of an increase in immunocompromised patients with diabetes mellitus, cancer, alcoholism, vascular insufficiencies, organ transplants, HIV infection, or neutropenia.

Necrotizing fasciitis These infections can be difficult to recognize in their early stages, but they rapidly progress. They require aggressive treatment to combat the associated high morbidity and mortality.

Purulent skin and soft tissue infections (SSTIs). Purulent skin and soft tissue infections (SSTIs). Mild infection: for purulent SSTI, incision and drainage is indicated. Moderate infection: patients with purulent infection with systemic signs of infection. Severe infection: patients who have failed incision and drainage plus oral antibiotics or those with systemic signs of infection such as temperature >38°C, tachycardia (heart rate >90 beats per minute), tachypnea (respiratory rate >24 breaths per minute) or abnormal white blood cell count (<12 000 or <400 cells/µL), or immunocompromised patients. Nonpurulent SSTIs. Mild infection: typical cellulitis/erysipelas with no focus of purulence. Moderate infection: typical cellulitis/erysipelas with systemic signs of infection. Severe infection: patients who have failed oral antibiotic treatment or those with systemic signs of infection (as defined above under purulent infection), or those who are immunocompromised, or those with clinical signs of deeper infection such as bullae, skin sloughing, hypotension, or evidence of organ dysfunction. Two newer agents, tedizolid and dalbavancin, are also effective agents in SSTIs, including those caused by methicillin-resistant Staphylococcus aureus, and may be approved for this indication by June 2014. Abbreviations: C & S, culture and sensitivity; I & D, incision and drainage; MRSA, methicillin-resistant Staphylococcus aureus; MSSA, methicillin-susceptible Staphylococcus aureus; Rx, treatment; TMP/SMX, trimethoprim-sulfamethoxazole. Dennis L. Stevens et al. Clin Infect Dis. 2014;cid.ciu296 © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Invasive Group A Streptococcal Infections Exotoxin A, superantigen Figure 21.8

Erysipelas Presentation: erythematous patch with a distinctive raised, indurated advancing border. Affected skin is very painful and is warm to touch. Freq. associated with fever , HA and leukocytosis >20,000. Face and Legs are most common sites. Involves superficial dermal lymphatics Cause: Group A strep., (Group B in newborns) Differential: Contact derm: more itching little pain. Scarlet fever: widespread punctate erythema Malar rash of Lupus and Acute tuberculoid Leprosy: Absence of fever pain and leukocytosis. Treatment: Systemic PCN for 10 days.

Erysipelas

Erysipelas

Streptococcal Toxic Shock Syndrome M proteins Complex with fibrinogen Binds to neutrophils Activates neutrophils Release of damaging enzymes Shock and organ damage

Infections by Pseudomonads Pseudomonas aeruginosa Gram-negative, aerobic rod Pyocyanin produces a blue-green pus Pseudomonas dermatitis Otitis externa, or “swimmer’s ear” Post-burn infections Opportunistic Hot-tub folliculitis

Infections by Pseudomonads Hot Tub Folliculitis Hot tub folliculitis is an infection of the hair follicles caused by the bacteria Pseudomonas aeruginosa. This bacteria is commonly found in contaminated whirlpools, hot tubs, water slides, physiotherapy pools, or even loofah sponges

Folliculitis and Furuncle Folliculitis Folliculitis is an infection that is localized to the hair follicle. A folliculitis looks like small, yellow pustules that are confined to the hair follicle. Furuncle A furuncle is an infection of the pilosebaceous unit, therefore is more extensive than a folliculitis because the infection also involves the sebaceous gland. Frequently occurs on the neck, face, armpits, and buttocks.

folliculitis staphylococcal pustulosis furuncle carbuncle

Carbuncle A carbuncle can simply be defined as an multiple furuncles grouped together. A carbuncle usually involves the deeper layers of the skin - the subcutaneous fat. It looks like a large, red nodule that is hot and may have visible layers of pus just beneath the surface of the skin

Folliculitis and Furuncle

Cellulitis Cellulitis is a bacterial infection of the deeper layers of the skin, the dermis and the subcutaneous tissue. In adults and children, cellulitis is most often caused by Streptococcus and Staphylococcus aureus bacteria. Sometimes Haemophilus influenzae type B can cause cellulitis in children younger than 3, but this has become less common because of vaccination.

Cellulitis

Impetigo Superficial infection usually staphylococcal (nose) but can also involve Streptococcus pyogenes (urt) Friable, golden crusts over erythematous skin

Buruli Ulcer Caused by Mycobacterium ulcerans Deep, damaging ulcers Exceeds incidence of leprosy

Classifications of Acne Comedonal (mild) acne Inflammatory (moderate) acne Nodular cystic (severe) acne

Comedonal Acne Mild Treatment Sebum channels blocked with shed cells Topical agents Salicyclic acid preparations Retinoids Adapalene

Inflammatory Acne Propionibacterium acnes Gram-positive, anaerobic rod Treatment Preventing sebum formation (isotretinoin) Antibiotics Benzoyl peroxide to loosen clogged follicles Visible (blue) light (kills P. acnes)

Nodular Cystic Acne Severe Treatment Isotretinoin Figure 21.9

Fungal Diseases of the Skin and Nails Learning Objectives Differentiate cutaneous from subcutaneous mycoses, and provide an example of each. List the causative agent and predisposing factors for candidiasis.

Cutaneous Mycoses Dermatomycoses Also known as tineas or ringworm Metabolize keratin

Dermatomycoses Figure 21.16

Cutaneous Mycoses Genera of fungi involved Treatment Trichophyton: Infects hair, skin, and nails Epidermophyton: Infects skin and nails Microsporum: Infects hair and skin Treatment Topical miconazole Topical allylamine

Cutaneous Mycoses Tinea unguium Treatment Itraconazole Terbinafine

Subcutaneous Mycoses More serious than cutaneous mycoses Sporotrichosis Most common U.S. disease of this type Sporothrix schenchii enters puncture wound Treated with potassium iodide (KI)

Candidiasis Candida albicans (yeast) Candidiasis may result from suppression of competing bacteria by antibiotics Occurs in skin and mucous membranes of genitourinary tract and mouth Thrush: An infection of mucous membranes of mouth Topical treatment with miconazole or nystatin

Candida albicans Figure 21.17a

Case of Oral Candidiasis Figure 21.17b

Systemic Candidiasis Fulminating disease can result in immunosuppressed individuals Treatment: Fluconazole

Parasitic Infestation of the Skin Learning Objective List the causative agent, mode of transmission, clinical symptoms, and treatment for scabies and pediculosis.

Scabies Sarcoptes scabiei burrows in the skin to lay eggs Treatment with topical insecticides Figure 21.18

Pediculosis (Lice) Pediculus humanus capitis (head louse) P. h. corporis (body louse) Feed on blood Lay eggs (nits) on hair Treatment with topical insecticides Figure 21.19

Cutaneus larva migrans

TUS 2012 Aşağıdakilerden hangisinde dissemine kandidiazis görülme olasılığı diğerlerine göre en düşüktür? A) Kanser kemoterapisi alan hastalar B) Nötropenik hastalar C) Uzun süreli sistemik steroid tedavisi alan hastalar D) Total parenteral beslenen hastalar E) Kronik mukokütanöz kandidiazisli hastalar

TUS 2012 Aşağıdakilerden hangisinde dissemine kandidiazis görülme olasılığı diğerlerine göre en düşüktür? A) Kanser kemoterapisi alan hastalar B) Nötropenik hastalar C) Uzun süreli sistemik steroid tedavisi alan hastalar D) Total parenteral beslenen hastalar E) Kronik mukokütanöz kandidiazisli hastalar

TUS 2012 “Hot-tub follikülit” etkeni aşağıdakilerden hangisidir? A) Klebsiella pneumoniae B) Streptococcus pyogenes C) Pseudomonas aeruginosa D) Staphylococcus aureus E) Candida albicans 

TUS 2012 “Hot-tub follikülit” etkeni aşağıdakilerden hangisidir? A) Klebsiella pneumoniae B) Streptococcus pyogenes C) Pseudomonas aeruginosa D) Staphylococcus aureus E) Candida albicans 

TUS 2012 Aşağıdakilerden hangisi, uyuz tedavisinde topikal olarak kullanılmamaktadır? A) Permetrin    B) Sülfür C) Benzil benzoat   D) Krotamiton E) İvermektin

TUS 2012 Aşağıdakilerden hangisi, uyuz tedavisinde topikal olarak kullanılmamaktadır? A) Permetrin    B) Sülfür C) Benzil benzoat   D) Krotamiton E) İvermektin

TUS 2012 Otuz beş günlük bir kız bebek öksürük ve solunum zorluğu yakınmalarıyla getiriliyor. Öyküsünden vajinal yolla zamanında doğduğu ve izleminde bilateral pürülan konjunktivit saptandığı öğreniliyor. Bu bebekte etken olarak öncelikle aşağıdakilerden hangisi düşünülmelidir? A) Streptococcus pyogenes B) Chlamydia trachomatis C) Mycoplasma pneumoniae D) Listeria monocytogenes E) Staphylococcus aureus

TUS 2012 Otuz beş günlük bir kız bebek öksürük ve solunum zorluğu yakınmalarıyla getiriliyor. Öyküsünden vajinal yolla zamanında doğduğu ve izleminde bilateral pürülan konjunktivit saptandığı öğreniliyor. Bu bebekte etken olarak öncelikle aşağıdakilerden hangisi düşünülmelidir? A) Streptococcus pyogenes B) Chlamydia trachomatis C) Mycoplasma pneumoniae D) Listeria monocytogenes E) Staphylococcus aureus

TUS 2012 Üç yaşında bir kız çocuk 3 gündür devam eden 39-40°C ye varan ateş, boğaz ağrısı ve boyunda bezeler nedeniyle getiriliyor. Fizik muayenede eksüdatif tonsillit ve splenomegali saptanıyor. Laboratuar incelemelerinde AST ve ALT düzeylerinde normalin üst değerinin iki katı yükselme gözleniyor. Bu çocuk için en olası tanı aşağıdakilerden hangisidir? A) Grup A streptokok enfeksiyonu B) 6. hastalık C) Kawasaki hastalığı D) Enfeksiyöz mononükleoz E) Difteri

TUS 2012 Üç yaşında bir kız çocuk 3 gündür devam eden 39-40°C ye varan ateş, boğaz ağrısı ve boyunda bezeler nedeniyle getiriliyor. Fizik muayenede eksüdatif tonsillit ve splenomegali saptanıyor. Laboratuar incelemelerinde AST ve ALT düzeylerinde normalin üst değerinin iki katı yükselme gözleniyor. Bu çocuk için en olası tanı aşağıdakilerden hangisidir? A) Grup A streptokok enfeksiyonu B) 6. hastalık C) Kawasaki hastalığı D) Enfeksiyöz mononükleoz E) Difteri

TUS 2012 Aşağıdaki etkenlerden hangisi en ciddi ophthalmia neonatorum formuna neden olur? A) Chlamydia trachomatis B) Herpes simpleks virusu C) Sitomegalovirus D) Staphylococcus aureus E) Neisseria gonorrhoeae

TUS 2012 Aşağıdaki etkenlerden hangisi en ciddi ophthalmia neonatorum formuna neden olur? A) Chlamydia trachomatis B) Herpes simpleks virusu C) Sitomegalovirus D) Staphylococcus aureus E) Neisseria gonorrhoeae

TUS 2013 Aşağıdaki bulaşıcı hastalık - kontrol programı eşleştirmelerinden hangisi yanlıştır? A) Kızamık - Eliminasyon B) Neonatal tetanoz - Eradikasyon C) Kızamıkçık - Eliminasyon D) Polio - Eliminasyon E) Tüberküloz - Hastalık kontrolü

TUS 2013 Aşağıdaki bulaşıcı hastalık - kontrol programı eşleştirmelerinden hangisi yanlıştır? A) Kızamık - Eliminasyon B) Neonatal tetanoz - Eradikasyon C) Kızamıkçık - Eliminasyon D) Polio - Eliminasyon E) Tüberküloz - Hastalık kontrolü

TUS 2013 Aşağıdaki mikroorganizmalardan hangisi, sağlam kornea epitelini geçemez? A) Neisseria gonorrhoeae B) Neisseria meningitidis C) Corynebacterium diphtheriae D) Haemophilus influenzae E) Streptococcus pyogenes

TUS 2013 Aşağıdaki mikroorganizmalardan hangisi, sağlam kornea epitelini geçemez? A) Neisseria gonorrhoeae B) Neisseria meningitidis C) Corynebacterium diphtheriae D) Haemophilus influenzae E) Streptococcus pyogenes

TUS 2013 Stafilokokkal toksik şok sendromunda, aşağıdaki klinik örneklerden hangisinde Staphylococcus aureus üreyebilir? A) Dışkı B) Kemik iliği C) Beyin omurilik sıvısı D) Vajen E) Nazofarenks

TUS 2013 Stafilokokkal toksik şok sendromunda, aşağıdaki klinik örneklerden hangisinde Staphylococcus aureus üreyebilir? A) Dışkı B) Kemik iliği C) Beyin omurilik sıvısı D) Vajen E) Nazofarenks

TUS 2013 Wright veya Giemsa ile boyandığında ortaya çıkan Donovani cisimciği aşağıdaki mikroorganizmalardan hangisinin varlığında görülür? A) Neisseria gonorrhoeae B) Chlamydia trachomatis C) Treponema pallidum D) Klebsiella granulomatis E) Candida glabrata

TUS 2013 Wright veya Giemsa ile boyandığında ortaya çıkan Donovani cisimciği aşağıdaki mikroorganizmalardan hangisinin varlığında görülür? A) Neisseria gonorrhoeae B) Chlamydia trachomatis C) Treponema pallidum D) Klebsiella granulomatis E) Candida glabrata

TUS 2015

TUS 2015

TUS 2015

TUS 2015