Bacterial skin and muscle infections: Lecture 34

Staphylococcus aureus

Golden yellow colonies on agar. Resistant to drying/heat. Fomites+. Protein A. Exfoliatin. Beta-lastamase plasmid. Tolerance to some antibiotics. Superantigens (enterotoxins) A-F. Folliculitis, boils, cellulitis, SSS, TSS. Catalase positive. coagulase

Protein A

S. aureus cell wall component. Binds to Fc portion of IgG.


S. aureus exfoliative toxin


S. aureus. Minor infection in and around the hair follicles. Surrounding induration and redness. Localized infection.


(boil). S. aureus. Originates as superficial infection (around foreign body or hair follicle. Organisms protected against host defenses. Multpily and spread locally. Fibrin deposited. Site is walled off. Yellow creamy pus formation.


S. aureus. Clusetered boils -> multifocal infection -> abscesses. Larger and deeper than boils. Can lead to bacteremia. Both boils and carbuncles may require debridement and antibiotic therapy.


S. aureus. Acute inflammatory process. Infection of cutaneous fat. Originates from trauma, boils or ulcers. S. aureus > 90% of cases. Occasionals GAS. Trauma, burns, surgery...

anaerobic cellulitis

C. perferingens. Bacterial spread along tissue fascia. No muscle invasion

Toxic shock syndrome

30-40% nasal carriage of S. aureus in general population. Organism may be undetectable. TSS: absorption of S. aureus toxin from initial site of infection and transport via blood. TSST-1. Severe shock (<48hours) w/ renal hepatic damage. Surface areas of skin start pealing. 2 forms: menstrual associated w/ super absorbent tampons. Non-menstruals: associated w/ infected surgical wounds, nasal tampons, puerperal sepsis. Fever > 102 degrees, vomitting, sore throat, myalgia, diffuse macular rash, hypotension, diarrha. Age and sex


Pyogenic superantigen

Diagnosis of TSS

Abrupt fever. Take cultures: S. aureus in grape-like clusters, catalase+, coagulase+

Scalded skin syndrome

S. aureus. SSSS. Most common newborns. Children < 5 years of age. Exofliatin. Splits epidermis by cleaving desmosomes present in stratum granulosum. Erythema around mouth that spreads over the whole body. Peel extremely easily.

Nikolsky's sign

Pealing skin in adults. Sign of exfoliatin

Streptococcus pyogenes

Forms chains on agar. Encapsulated (hyaluronic acid). Present on human skin and mucous membranes. Skin infections = typical. Beta hemolytic group A. virulence factor: M protein. Streptococcal pyrogenic exotoxins: A, B, and C. portal of entry determines clinical presentation. Facultative anaerobe

M protein

Component of pili. > 80 types. Binds fibrinogen -> dense coat – blocks complement deposition. Role in pathogenesis of rheumatic fever.


Spreading factor for S. pyogenes.


Fibrinolysin. Catalyses conversion of plaminogen to plasmin. Degradation of fibrin. Found in GAS.


Streptolysin O, streptolysin S (responsible for clear zone on BA plates)

Streptococcal pyrogenic exotoxins

A, B, and C antigenically distinct


Tender, superficial erythematous and edematous lesions especially on face or lower limbs. Pain and lymphadenopathy. Fiery red and rapidly advancing erythema. Unlike cellulitis, clearly delineated margins. Dermis


Intraepidermal vesicles filled with exudate -> weeping and crusting lesions. Acquired through direct contact. Common in children. Peak incidence 2-5 years. S. pyogenes (classic cause) or S. aureus (bullous impetigo. Currently more clinical import.). May occasionally be followed by acute glomerulonephritis. epidemis

Scarlet fever

Erythrogenic toxin. Lysogenic phage encoded. Erythematous rash on neck trunk and extremities that fades and is followed by extensive desquamation. Strawberry tongue.

Streptococcal TSS

Fulminant infection; shock and multi-organ failure. Begin at site of trivial trauma. 30% mortality even w/ antibiotic treatment. Associated w/ shock, necrotizing fasiitis, myonecrosis, bacteremia. “flesh-eating bacteria”

Infective endocarditis

Primarily due to oral streptococci (prev: viridans and streptococci). Account for ~70% of cases Strep and 50% of those are S. viridans. Other causes: Enterococcus faecalis, S aureus (IV drug users). Infection usually occurs on abnormal valves. Fatal w/o treatment

Subacute bacterial endocarditis

Microorganism enters blood --> heart --> lodge on heat tissue; multiply --> become trapped in blood clots. Fever --> heart murmur. Non-specific symptoms: anorexia, malaise, chills, nausea, vomitting, night sweats

Necrotizing fasciitis

Deep local invasion of tissues and tissue necrosis. Acute infection: rapid patient deteriation. Symptoms: toxic shock-like syndrome, fever, hypotension, multi-organ involvement high mortality. Local and systemic antibiotics and surgery. Polymicrobial, Streptococcal, Clostridial myonecrosis. Dark blue-red fluid filled blisteres. Pseudomonas aeruginosa.

Gas gangrene

Clostridium perfringens. Obligate anaerobe. Infection develops in areas w/ poor blood supply. Buttocks, perineum. Exogenous or endogenous (from faecal flora). Accumulation of CO2 and H2 in tissues. Less likely than localized cellulitis. Dead and dying tissue further compromise circulation. Fever, sweats, hypotension. Death from shock and renal failure. ~12 soluble antigens. Degradative enzymes. Alpha-toxins = lechithinase.

Naglar reaction

Clearing zone around microorganism if toxin is present.

Diagnosis of gas gangrene

Necrosis. G- organisms. Recent injury/surgery. Crepitis upon palpitation


Propionibacterium acnes. Gram + bacillus. Anaerobic. Member of normal skin flora. Found in sebaceous glands. Virulence factor: lipases hydrolyze sebum triglycerides --> fatty acids --> inflammation. Tetracycline, erytrhomycine


Myobacterium leprae

Cutaneous anthrax

Bacillus anthracis

Cutaneous diphtheria

Clostridium diphtheriae


Fungal Skin and muscle infections: lecture 35


10% KOH. Morphology is important: Sabouraud's agar (only glucose and peptones w/ pH 5.6). serology: detection of fungal specific antibodies.

Superficial mycoses

Limited to outer layer of skin and hair. Mild; minimal or no inflammatory response. Easy to diagnose and responds to therapy

Cutaneous mycoses

Caused by dermatophytes. Can be acute or chronic. More difficult to treat. Called “tineas”; grouped according to body site

Subcutaneous mycoses

Usually associated w/ trauma. Can mimic bacterial diseases. Don't respond well to therapy and may require excision.

Systemic mycoses

Invade organs of body. Can be due to primary pathogens or opportunistic pathogens.

Pityriasis versicolor

Tinea versicolor, tinea flava, liver spots. Superficial mycoses. Pityosporum orbiculare (part of normal flora). Usually confined to trunk or proximal parts of limbs: chest, abdomen, back, upper limbs. Hypo or hyper-pigmented macules. Mild; non-inflammatory; non-itchy; sharply marginated lesions. Tx: selenium sulfide; topical azoles. Spaghetti and meatballs.

Tinea nigra

Hortaea werneckii. Dark brown to black painless non-scaly elevated lesions (mottled areas of skin). Palms of hands or soles of feet. Primarily in the tropics. Tx: Keratolytic solutions; sialicyclic acid or azoles

Black piedra

Piedra hortae. Hard gritty black nodules (hyphal mass and capsule) usually on scalp hair. Tropical areas of Asia, Africa, South America. Diagnosis by direct microscopic examination of hair. Culture on Sabouraud's agar. Tx: Removal of hair; topical antifungal

White piedra

Trichomycosis. Tinea nodosa. Trichosporon beigelii. Infection of hairs on scalp, face and genital area. Soft white/creamy yellow granules form a sleeve or collar around the hair or shaft. World wide distribution


Keratin-loving (invade skin, hair and nails). Common. Annular, scaly patch with raised margins, itchy, skin becomes dry and may crack, infection of hair: may result in hair loss, infection of nails: tend to be chronic. Varying degrees of inflammation (species; individual).

Pathogenesis of dermatophytoses

Active disease leads to inflammatory reaction in underlying epidermis and dermis. Scaling due to increased epidermal turnover and invasion of toe nails, hair and hair follicles. Systemic infections are rare due to temperature restriction. Tinea pedis, tinea corporis, tinea capitis, tinea unguium

Etiologic agents

Microsporum – invades hair and skin


Invades skin and nails


Invades skin, hair and nails


Character ring shape – grow outward in centrifugal pattern. Among most common skin disorders of children < 12 years of age. All treatment requires removal of dead skin and dead epithelium

Tinea corporis

Ringworm. Most common in 5-10 year olds. 3:1 males:females. T. rubrum, T. mentogrophytes. Includes tinea cruris: ringworm of the groin - “jock itch”. Arms, legs, check, back, etc.

Tinea pedis

Athlete's foot. Predominant in later life. 6:1 males:females. Trichophyton rubum, Trichophyton mentogrophytes, Epidermophyton floccosum. Can progress from chronic infection (cracking and peeling of skin) to acute ulcerative form. Tx: itraconazole.

Tinea capitis

Ringworm of the scalp. T. tonsurans, M. canis, M. audouinii. Non-inflamed, scaly red lesions – sometimes w/ hair loss. Deep ulcers may occur due to inflammatory reaction --> heal with scarring and permenent hair loss. Tx: griseofulvin: 4-6 weeks; shampoo or creams with miconazole.

Tinea unguium

Infection of nails (thickened & discoloured). Can be chronic, with long term persistence. Most common etiologic agent = T. rubrum. Characteristics: discolouration of subungual tissue, hyperkeratosis and discolouration of nail plate, direct infection of nail plate (uncommon). Tx: oral intraconazole (extended period)

Way to remember


Dermatophytid reaction

Erythema w/ vesiculation and/or desqumation along sides of hands and feet. Type IV hypersensitivity due to circulating fungal antigens. Non-active infection. Examine elsewhere on body for evidence of fungal infection

Candida albicans

Non-dermatophytic fungus. Microflora of oral cavity, lower GIT, female genital tract. Various types of cutaneous candidiasis: intertriginous, generalized, paronchia, onychomycosis, diaper disease


Inflammation of the nail fold w/ seperation of the skin from the proximal portion of the nail.

Intertriginous candidiasis

Usually occurs in: individuals w/ metabolic disorders. Obese individuals (continuously moist folds of skin). Areas that are continually moist, e.g., surgical dressings, diapers.

Initial lesions

Erythematous papules or confluent areas, tenderness, erythema, fissures of skin. Infection usually confined to chronically irritated area (but can spread). Chronic mucocutaneous candidiasis (rare) – skin mucous membranes, hair and nails become infected. Tx: nystatin, clotrimazole; measures to decrease moisture and chronic trauma

Subcutaneous mycoses

Bacterial infections, e.g. Due to streptococci, nocardi, may mimic clinical and pathological manifestations. Can be attributed to a number of different fungal species. Relatively rare. Can be difficult to eradicate and may require surgical intervention


Verrucous dermatitis. Phialophora, Cladosporium. Found in decaying vegetable matter and rotting wood. Exposure is via implantation (e.g. Punctured wounds to feet). Common in tropical areas. Usually local infection; dissemination via blood is rare. Original lesion = small, raised, violet papule. Additional lesions develop with time. Hard, dry lesions, raised 1-3mm above skin. Diagnosis: 10% KOH mount: look for copper colored schlerotic bodies, brown pigmented hyphae. Culture on Sabouraud's agar. Treatment: 5-flucytosine & excision


Sporothrix schenckii. Soil, plants, wood and moss – from splinters, thorns, etc... dimorphic: small budding yeast at 37C. High incidence in rural South America. Tx: oral KI (given in milk) oral itraconazole. Local infection --> subcutaneous tissues and regional lymph nodes --> 1 week to 6 months incubation --> formation of subcutaneous nodules and necrotic ulcer --> invasion of blood and spread --> pulmonary sprotrichosis


Cryptococcus neoformans. Widely distributed in soil, often found in pigeon droppings. Large polysaccharide capsule. Usually causes infection of lungs, but skin infections are also common. Diagnosis by latex agglutination test, dilute india ink and microscopy (diagnostic in 50% of cases). Tx: combined amphotericin and flucytosine


Mycetoma due to fungus = unusual infection associated w/ trauma to feet, lower extermities, hands. Etiologic agent (USA): Petriellidium boydii. Local swelling, suppuration and abscess formation, granulomas, draining sinuses. Treatment is often difficult: surgical debridement; long term chemotherapeutic agents.