cumitech 23: infections of the skin and subcutaneous tissues

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Page 1: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

CUMITCCH 23

Page 2: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

Cumitech I,4 * Blood Cultures II * June 1982 Cumttech ?A * Laboratory Diagnosis of Urmary Tract Infections * March 1987 Cumitech 3 * Practical Qualrty, Control Procedures for the Clmical Microbiology Laboratory -

September 1976 Cumitech 4 * Laboratory Diagnosis of Gonorrhea * October 1976 Cumitech 5 * Practical Anaerobic Bacteriology * April 1977 Cumitech 6 * Neu De\,elopments in Antimicrobial Agents Susceptibility Testmg * September

1977 Cumttech 7A * Laboratory Diagnosis of Lo\+ er Resptratory Tract Infections * September 1987 Cumitech 8 * Detection of Microbial Antigens by Counterimmunoelectrophoresis * December

1978 Cumttech 9 * Collectton and Processing of Bacteriological Specimens * August 1979 Cumitech 10 * Laboratory Diagnosis of Upper Respiratory Tract Infections * December 1979

Cumitech 11 * Practical Methods of Culture and Identification of Fungi in the Climcal

hlicrobiology Laboratory * .4ugust 1980 Cumitech 12 * Laboratory Dtagnosis of Bacterial Diarrhea * October 1980 Cumitech 13 * Laboratory Dtagnosts of Ocular Infections * May 1981 Cumitech 14 * Laboratory Diagnosis of Central Nervous System Infections * January 1982 Cumitech 15 * Laboratory Diagnosis of Viral Infections * March 1982 Cumitech 16 * Laboratory Dtagnosis of the Mycobacterioses * March 1983

Cumitech 17 * Laboratory Diagnosis of Female Genital Tract Infections * August 1983 Cumitech 18 - Laboratory Diagnosis of Hepatitis Viruses - January 1984 Cumitech 19 * Laboratory Diagnosis of Chlamydial and Mycoplasmal Infections * August 1983 Cumitech 20 * Therapeuttc Drug Momtoring: Antimicrobial Agents * October 1984 Cumitech 21 * Laboratory Diagnosis of Viral Respiratory Disease * March 1986

Cumttech 22 + Immunoserology of Staphylococcal Disease * August 1987

Cumitechs should be cited as follows, e.g.: Simor, A. E., F. J. Roberts, and J. A. Smith. 1988. Cumitech 23, Infections of the skin and subcutaneous tissues. Coordinating ed.. J. A. Smith. American

Society for Microbiology, Washington, D.C.

Editorial Board for ASM Cumitechs: Steven C. Specter. Chapman: Carl Abramson. Willram J Martone, John E. McGowan, Jr, Glenn D. Roberts, James W. Smrth, John A. Smrth, Thomas J Trnghrtella,

and Alrce S. Werssfeld

The purpose of the Cumitech series IS to provide consensus recommendations by the authors as to appropriate state-

of-the-art operating procedures for clinlcal microbiology laboratories which may lack the facilities for fully evaluating

routine or new methods.

TQp, ~QL%!uP,~ gx~,n. xe oat prQpQsed as “standard” methods.

Copyright % 1988 Amencan Society for MIcrobiology

1913 I St NW

Washmgton. DC 20006

Page 3: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

INFECTIONS OF THE SKIN AND SUBCUTANEOUS TISSUES

ANDREW E, SIMOR, Department of Microbiology, Mount Sinai Hospital, and University of Toronto, Toronto, Ontario M5G 1x5, Canada

FREDERICK J. ROBERTS, Division of Microbiology, Vancouver General Hospital, and University of British Columbia, Vancouver, British Columbia VSZ lM9, Canada

JOHN A. SMITH, Division of Microbiology, Vancouver General Hospital, and University of British Columbia, Vancouver, British Columbia V5Z IM9, Canada

COORDINATING EDITOR

JOHN A. SMITH, Division of Microbiology, Vancouver General Hospital, and University of British Columbia, Vancouver, British Columbia V5Z lM9, Canada

The skin (Fig. 1) is the most accessible organ of the body, the one most readily traumatized and therefore the one subjected most fre- quently to the risk of infection. Composed of a superficial zone called the epidermis and a deeper zone called the dermis, it is an organ that is richly endowed with specialized struc- tures and functions. Body temperature and fluid control are influenced by skin, as are sensory functions such as touch and pain. Hair follicles, sebaceous glands, and sweat glands open to the skin surface. Beneath the dermis is a layer of subcutaneous fat, below which sit the thin fascial membranes that cover muscles, ligaments, and other connective tissues. Fas- cial planes create spaces in various parts of the body, including the head and neck, fingers, hands, and feet. The fascia is a barrier that determines the extent to which infections may spread but may also create therapeutic chal- lenges, due to impenetrability, which may have to be met surgically.

This Cumitech is concerned with some of the common infections that involve skin and subcu- taneous tissues. This is a complex subject in- volving a great diversity of organisms and of etiological and pathogenetic mechanisms. These infections are classified as primary and second- ary. Primary infections occur de novo in patients with no obvious portal of entry, e.g., erysipelas. Secondary infections arise as complications of injury to the skin such as abrasions, surgical trauma, or penetrating wounds. These infections are either monomicrobial, as in staphylococcal wound infection, or polymicrobial, as in some gangrenous conditions caused by microaerophi- lit streptococci and anaerobes. Secondary infec- tions may be localized or extensive, depending on the extent of the underlying disease or pre- cipitating trauma.

Infections may also be acute or chronic. An acute staphylococcal furuncle lasts a few days, whereas some chronic fungal infections may last for months or years. Infections in which the primary focus is in deeper structures may ex- hibit striking cutaneous manifestations, further complicating classification of infections, e.g., toxic shock syndrome, meningococcal septice- mia, and many other infections.

Clinical classification was adopted as the method for organizing the material for this CU- mitech. To this end we selected those diseases that may be classified as superficial erythema- tous infections, ulcers and nodules, sinus tracts, burns, simple postoperative wounds, compli- cated wound infections, and bites. Each class of infection has been highlighted with regard to the main clinical features, the common causative organisms, and a practical approach to labora- tory diagnosis.

We have purposely excluded the diseases that either are systemic or have a noncutaneous pri- mary focus. Cutaneous manifestations of endocar- ditis, ecthyma gangrenosa, secondary syphilis, and viral exanthemata are some examples of this large group of diseases. Similarly, we have ex- cluded infections in which disease affecting the skin is mediated by toxins, as well as parasitic infestations and ophthalmic and genital infections. The examination of all of these subjects would require a volume more extensive and diverse than is intended for the Cumitech format.

Laboratory procedures that are described in another Cumitech are not duplicated in this volume.

SUPERFICIAL ERYTHEMATOUS LESIONS The common infecting microorganisms and

laboratory diagnostic methods in superficial ery- thematous infections are listed in Table 1.

1

Page 4: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

SIMOR ET AL.

Epiderrnls

Dermis

Subcutaneous fat

Fascia

MUSCl9

FIG. 1. Section through normal skin.

Erysipelas and Cellulitis Erysipelas is a superficial infection of the skin,

usually caused by group A streptococci, al- though rare cases due to group C or group G streptococci have also been described. The in- fection primarily involves the dermis and the most superficial parts of the subcutaneous tis- sues, with prominent involvement of superficial lymphatics. Erysipelas presents as a painful, fiery red, edematous, and indurated area of skin, occasionally with small vesicles or bullae on the surface. There may be a “peau d’orange” (or- ange rind-like) appearance due to the marked superficial cutaneous edema. A key clinical fea- ture is the raised border of the skin lesion that is sharply demarcated from adjacent normal or uninvolved skin. The acute onset of fever and chills is prominent, and regional lymphadenop- athy is often present.

Cellulitis is a diffuse, spreading infection in- volving the loose connective tissue of deeper layers of the dermis. It is characterized by local pain, tenderness, erythema, and edema, associ- ated with fever, chills, and regional lymphade- nopathy. Unlike erysipelas, the margins of an area of cellulitis are ill defined, not elevated or sharply demarcated. Group A streptococci and

CUMITECH 23

Staphylococcus aureus are considered to be the most common etiological agents. Aeromonas and Vibrio species may cause an acute cellulitis following introduction of the organism through a wound or laceration sustained while swimming in fresh or salt water. Haemophilus influenzae cellulitis is a relatively uncommon but distinc- tive form of infection often associated with bacteremia and typically affecting children 6 months to 3 years of age (31).

The diagnosis of cellulitis or erysipelas can generally be made clinically, and knowledge of the usual bacterial pathogens can guide empiric antimicrobial therapy. The treatment of choice for erysipelas is penicillin (erythromycin for a patient with penicillin allergy). Empiric treat- ment of cellulitis should be with a penicillinase- resistant penicillin (e.g., cloxacillin) or a cepha- losporin effective against both Streptococcus pyogenes and S. aureus. In children, therapy should include antimicrobial coverage for H. in.uenzae. The choice of antimicrobial therapy may be modified in light of subsequent microbi- ological findings.

Laboratory Anecdotal reports have suggested the potential

value of needle aspiration for the bacteriological diagnosis of soft tissue infections (40). The tech- nique for aspiration involves disinfecting the site and aspirating the advancing margin of erythema with a 22. or 23.gauge needle attached to a 3- or 5-ml syringe. If the initial aspiration fails to pro- vide material for culture, 0.1 to 0.5 ml of sterile, nonbacteriostatic isotonic saline may be injected subcutaneously, followed immediately by a repeat attempt at aspiration without removing the needle from the injection site. If, after this, no fluid is recovered, the needle and syringe may be rinsed with broth by drawing the culture medium through the needle into the syringe, and the tip of the

TABLE 1. Superficial erythematous infections

Diseases and syndromes Common causative organisms Laboratory diagnostic methods

Ery sipelas Cellulitis

Erysipeloid Impetigo Folliculitis , furunculosis,

carbuncles Paronychia Whitlow

Superficial mycoses

Erythrasma

Group A streptococci Group A streptococci, S. aureus

E. insidiosa Group A streptococci, S. aureus S. aureus, P. aeruginosa,

Proteus spp. S. aureus, Candida spp. S. aureus, herpes simplex virus

Candida spp., E. floccosum, Trichophyton sp., Microsporum

C. minutissimum

SP-

Gram stain, culture on blood agar and chocolate agar, MacConkey agar, Trypticase soy broth

Culture on blood agar Gram stain, culture on blood agar Gram stain, blood agar,

MacConkey agar Gram stain, culture on blood agar Gram stain, culture on blood agar, virus

culture, fluorescent-antibody staining, electron microscopy

KOH preparation, culture on Sabouraud dextrose medium with chloramphenicol and cycloheximide

Wood’s lamp, Gram stain, tissue culture

Page 5: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

CUMITECH 23 SKIN AND SUBCUTANEOUS TISSUE INFECTIONS 3

needle may be streaked across the culture plate. Although advocated as a method for obtaining a bacteriological diagnosis (21), the value of needle aspiration in the management of erysipelas or cellulitis has not been clearly demonstrated. In retrospective reviews of cellulitis in adults, soft tissue aspiration yielded a positive culture in only 5 to 12.5% of specimens tested (14,15). A prospec- tive study of techniques for the microbiological evaluation of cellulitis in 50 adult patients found that only 4% of blood cultures, 10% of soft tissue aspirates, and 20% of punch skin biopsies were positive ( 19). In children with cellulitis, where infection is often due to H. influenzae type b, there may be a higher percentage of positive cultures of blood or soft tissue aspirate (12, 31). Aspirates should be cultured on blood agar, on chocolate agar, and in a broth such as Trypticase (BBL) soy broth.

Erysipeloid

A relatively uncommon nonsuppurative cellu- litis due to the gram-positive bacillus Erysipelo- thrix rhusiopathiae (E. insidiosa) is primarily seen as an occupational disease of fishermen, fish handlers, butchers, and abbattoir workers. The hands and fingers are the major sites of involvement. The lesion typically presents as a painful, purplish area of inflammation, with an erythematous advancing edge but central pallor. Unlike streptococcal or staphylococcal cellu- litis, local suppuration, fever, and constitutional symptoms are uncommon. Penicillin is the treat- ment of choice; erythromycin is a suitable alter- native in a patient with penicillin allergy.

Laboratory Gram stain or culture of superficial wound

drainage is usually negative. The bacteriological diagnosis of erysipeloid can be confirmed by culture of a full-thickness skin biopsy taken at the margin of the lesion. Details regarding the isolation and identification of E. rhusiopathiae have been described previously (42). Briefly, the biopsy should be placed in 5 ml of Trypticase soy broth, incubated aerobically or in CO, at 35 to 37”C, and subcultured onto blood agar daily for 5 days or until a positive subculture is obtained.

Impetigo Impetigo is a superficial intra-epidermal infec-

tion of the skin, producing erythematous lesions that may be either bullous or nonbullous. Non- bullous impetigo is usually caused by group A streptococci, whereas S. aureus has been asso- ciated with the bullous form of disease. The lesions of nonbullous impetigo begin as small, erythematous papules, which then form vesicles (l- to 2-cm diameter). Within a few davs. the

vesicles pustulate and rupture. The purulent discharge dries, forming characteristic, thick, amber- or honey-colored crusts surrounded by an erythematous margin or halo. Cultures of the lesions yield group A streptococci in pure cul- ture or mixed with S. aureus, although the staphylococci are generally considered to be “secondary invaders” rather than primary pathogens. Impetigo occasionally has been at- tributed to infection due to group C or G strep- tococci. Recommended therapy is with penicil- lin (erythromycin for a patient with penicillin allergy).

Bullous impetigo, usually caused by S. au- reus, is less common than streptococcal impe- tigo and usually occurs in neonates and infants. The lesions begin as vesicles and then typically form groups of superficial, flaccid bullae (0.5- to 3.0.cm diameter) with minimal or no surround- ing erythema. The bullae are thin walled and rupture easily, revealing an underlying patch of raw skin resembling a second-degree burn. The exudate may be serous or purulent and forms a thin brown crust on drying. The treatment of choice is with a penicillinase-resistant penicillin pending bacteriological results.

Laboratory The diagnosis of impetigo is generally made

by noting the typical clinical appearance of the lesions. Bacteriological confirmation is not usu- ally required, but after* the skin lesion has been cleaned with 70% alcohol, the crust may be removed and the base of the lesion cultured. Serological evidence of recent group A strepto- coccal infection may occasionally be useful for confirming the diagnosis retrospectively. The detection of antibody to streptococcal DNase B is a more sensitive indicator of group A strepto- coccal skin infection than is the anti-streptolysin 0 titer, probably because of inhibition of strep- tolysin 0 by lipids in the skin at the infection site. Culture on blood agar is adequate.

Folliculitis, Furunculosis, and Carbuncles Folliculitis, furunculosis, and carbuncles are

localized cutaneous abscesses that are distin- guished by their size and extent of subcutaneous involvement (Fig. 2).

Folliculitis Folliculitis is infection and inflammation of

hair follicles usually precipitated by blockage of the follicle or by minor local trauma (Fig. 2). The infection is characterized by dome-shaped pap- ules or pustules, pierced by a hair and sur- rounded by a rim of er ythema. The inflammation is nearly always due to S. aureus, and although the etiology of the folliculitis may be confirmed bv culture of pus or exudate from the lesion. this

Page 6: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

4 SIMOR ET AL. CUMITECH 23

FIG. 2. Folliculitis in a hair follicle.

is not usually necessary. Treatment with local measures, such as saline compresses and topical antibiotics (e.g., clindamycin), is usually suffi- cient.

Other, much less common, causes of follicu- litis include gram-negative folliculitis due to members of the family Enterobacteriaceae (es- pecially Proteus species). This may occur in patients with acne vulgaris who have received oral antibiotics for prolonged periods of time. Recently, outbreaks of folliculitis associated with the use of whirlpools, swimming pools, and hot tubs contaminated with large numbers of Pseudomonas aeruginosa have been recognized (16, 30). The cutaneous eruption consists of itchy, erythematous papules or papulopustules. The rash is not unique in appearance but does have a characteristic distribution, primarily in- volving buttocks, hips, thighs, and axillae. These are areas where apocrine sweat glands are located and areas which tend to be occluded when bathing suits are worn. In addition to the rash, many individuals complain of a low-grade fever, headache, malaise, earache (due to ac- companying otitis extema), and painful breasts (due to mastitis). The characteristic distribution of the rash in association with a recent history of exposure in a whirlpool, hot tub, or swimming pool is helpful in making the diagnosis. The illness may last several weeks, but is generally self-limiting with spontaneous healing, and no specific therapy is required.

Laboratory

In staphylococcal folliculitis, bacteria are usu- ally not seen on Gram-stained smear and cul- ture. However, in pseudomonal folliculitis, al- though P. aeruginosa may be cultured from larger pustules, cultures are often negative.

Furunculosis and Carbuncles

A furuncle is an abscess that begins in a hair follicle as a firm, tender, red nodule that be- comes painful and fluctuant. A carbuncle is

FIG. 3. Fur-uncle (boil) destroying tissue around a hair follicle.

deeper and more extensive, often presenting as multiple subcutaneous abscesses involving sev- eral hair follicles and sebaceous glands and which drain along hair follicles (Fig. 3 and 4). Carbuncles may be associated with fever and malaise and may be complicated by cellulitis or bacteremia. Both furuncles and carbuncles oc- cur on skin subject to friction and perspiration and where hair follicles are present (e.g., but- tocks, axillae, neck, and face). S. aureus is the most frequent pathogen. Treatment with warm compresses is usually adequate for small local- ized furuncles. Antistaphylococcal antibiotics, such as cloxacillin and clindamycin, may be required in the presence of fever or if there is surrounding cellulitis, especially if the fur-uncles or carbuncles are located about the mid-face.

Laboratory

The microbiological diagnosis can generally be made by culturing pus from the lesions aero- bically on blood agar and MacConkey agar at 35°C for 18 h.

Paronychia

Paronychia is a superficial infection of the nail fold that may be acute or chronic. Acute infec- tions are due to S. aureus, which may be cul- tured from purulent drainage. Treatment with warm compresses is usually adequate, although sometimes incision and drainage may be re- quired. Chronic paronychia is often associated with frequent immersion of hands in dishwater and is usually due to Candida species. Treat- ment of Cundida infection of the skin and nail

FIG. 4. Carbuncle, a complex of abscesses tiect- ing several hair follicles.

Page 7: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

CUMITECH 23 SKIN AND SUBCUTANEOUS TISSUE INFECTIONS 5

bed include elimination of the precipitating cause and a 2% solution of gentian violet in ethanol applied directly to the lesion. Other antifungal agents such as nystatin and clotrima- zole may be used.

Laboratory

The microbiological diagnosis may be con- firmed by culturing aspirated or drained pus aerobically on blood agar as described above.

Whitlow

Whitlow is a purulent lesion on the distal phalanx of a finger, often caused by a penetrat- ing wound by a small sharp object. S. aureus is often the cause. It should be noted that a similar lesion may be caused by herpes simplex virus and that herpetic whitlow is often misdi- agnosed as a bacterial paronychia. Clinical features in herpetic whitlow that help distin- guish it from pyogenic infection include the following: (i) medical, paramedical, or dental occupation; (ii) presence of “satellite” vesi- cles; (iii) pain disproportionate to physical findings; (iv) nontense pulp space; and (v) serous rather than purulent vesicular fluid. Treatment for staphylococcal infection is with a penicillinase-resistant penicillin (e.g., cloxa- cillin) or clindamycin. Herpetic whitlow may be treated with acyclovir.

Laboratory The bacteriological diagnosis may be con-

firmed by Gram stain and culture on blood agar. The virological diagnosis may be confirmed by viral culture of vesicular fluid, direct fluores- cent-antibody staining of epithelial cells from the base of the lesion, or electron microscopy.

Superficial Mycoses

Cutaneous fungal infections involve the kera- tinized layer of the stratum corneum, hair, or nails. They may be caused by dermatophytes, Candida species, or lipophilic yeasts. In general, dermatophytic skin infections due to Epider- mophyton jloccosum or Trichophyton or Mjcro- sporum species produce pruritic, scaly, erythe- matous lesions often with a characteristic “ringworm” appearance. Treatment with topi- cal antifungal medications (e.g., tolnaftate and imidazole derivatives) is usually adequate.

Candida albicans may colonize or infect skin or mucous membranes, especially if there is cutaneous maceration or altered host defenses ( g immunosuppression and diabetes mel- liusi. Superficial yeast infection, usually caused by Candida species, tends to occur in the groin, diaper, or inframammary areas. The affected skin is raw, moist, and erythematous, with small satellite papules or pustules.

Tinea (pityriasis) versicolor is an infection of the stratum corneum due to the lipophilic yeast Malassezia furfur. Typical lesions, especially involving the torso and upper limbs, are faintly erythematous or hypopigmented macules with a fine scale. Treatment is with 2.5% selenium sulfide (Selsun shampoo).

Laboratory If cutaneous fungal infection is suspected,

the lesion should be cleaned and scrapings from the active border of the lesion should be obtained. The scrapings should be suspended in potassium hydroxide and examined micro- scopically for the presence of hyphae. Derma- tophytes produce septate hyphae with arthro- spores, while M. furfur produces short hyphae with blastospores. If there is nail involvement, scrapings of debris or material beneath the nail plate are appropriate. Scalp lesions should be scraped with a scalpel blade to obtain frag- ments of hair for examination. Scrapings may be cultured on Sabouraud dextrose medium with chloramphenicol and cycloheximide to determine the fungal species. Such specimens should be handled as described previously (18). Wood’s light may reveal golden-yellow fluores- cence of lesions of tinea versicolor or hair infection due to Microsporum species or Tri- chophyton schoenleinii, which fluoresce bright yellow-green. Similarly, Wood’s lamp may be used to select hair for examination.

Erythrasma

Erythrasma is a chronic, superficial bacterial skin infection of the stratum corneum, often mistaken for a dermatophyte infection. It is caused by the diphtheroid Corynebacterium mi- nutissimum and presents with fine, scaly, red- dish-brown macules or plaques, especially in the toe webs or genitocrural areas. The rash may be asymptomatic or pruritic. Erythrasma should be treated with oral erythromycin.

Laboratory Wood’s lamp examination of lesions is diag-

nostic, revealing a characteristic coral red fluo- rescence, which is due to porphyrin production by the organism. A Gram-stained imprint of the skin surface or scales shows many small pleo- morphic gram-positive bacilli, coccobacilli, or filaments. A culture is rarely required to make the diagnosis, but the organism may be grown from skin scrapings in tissue culture medium containing fetal bovine serum (35).

ULCERS AND NODULES

The common organisms, syndromes, and lab- oratory methods used to investigate ulcers and nodules are listed in Table 2.

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6 SIMOR ET AL. CUMITECH 23

TABLE 2. Ulcers and nodules

Diseases and syndromes

Common causative organisms Laboratory diagonostic methods

Sporotrichoid lesion

Blastomycosis Cryptococcosis

Cutaneous diphtheria Anthrax Tularemia

S. schenckii, M. marinum, Nocardia species

B. derma titidis C. neoformans

C. diphtheriae B. anthracis F. tularensis

Histology (PAS and GMS stains”), Gram stain, acid-fast stain, biopsy culture on mycobacterial medium (e.g., 7H9 at 30 to 32”C), blood agar (sealed with Parafilm) for 4 weeks, Sabouraud dextrose with chloramphenicol and cycloheximide

Culture on blood agar and Sabouraud dextrose with chloramphenicol and cycloheximide, India ink stain for C. neoformans

Gram stain Culture on blood agar and tellurite blood agar Serum agglutinating antibody (fourfold rise in titer

over 2 weeks or single titer of ~1: 160 after 2 weeks of illness)

“PAS, Periodic acid-Schiff; GMS, Gomori-methenamine-silver.

In cutaneous ulcers there usually is a loss of epidermal and part of the dermal tissue (Fig. 5). Nodules are inflammatory foci in which the most superficial cutaneous layers are intact. A variety of bacteria and fungi cause ulcerative or nodular skin lesions or both following direct inoculation. Important examples include Corynebacterium diphtheriae, Bacillus anthracis, Francisella tu- larensis, Nocardia species, Mycobacterium ma- rinum, and Sporothrix schenckii. Alternatively, cutaneous infection may follow hematogenous dissemination to the skin from some other focus of infection. For example, Blastomyces derma- titidis and Cryptococcus neoformans cause pri- mary pulmonary infections which may be com- plicated by hematogenous dissemination to ex- trapulmonary sites, such as the skin and soft tissues, in 10 to 70% of cases. Microscopy and culture are the main methods of laboratory di- agnosis. However, serological testing is avail- able for certain organisms, including some fungi. These are usually carried out in reference labo- ratories and are not described in detail in this Cumitech.

Sporotrichoid Lesions

Sporotrichoid lesions are a distinctive form of ulceronodular infection with lymphatic involve- ment. Although classically associated with in- fection due to S. schenckii, lesions may also be seen with infection due to M. marinum or No- cardia species. These lymphocutaneous infec- tions begin with an ulcerated nodular lesion at the site of inoculation primarily on the extremi- ties, followed by the development of subcutane- ous nodules with overlying erythema and occa- sional ulceration proximally along lymphatics. Infection caused by S. schenckii, a dimorphic soil and plant fungus, often follows contact with thorny plants or sphagnum moss, with direct inoculation of spores into subcutaneous tissue.

M. marinum is a pathogen of both fresh- and saltwater fish, and human infection usually fol- lows superficial cutaneous injury in marine or tidal water, swimming pools, or tropical fish tanks. Although cutaneous infection due to No- cardia asteroides is usually a result of hemato- genous dissemination from a primary pulmonary focus of infection, primary cutaneous nocardi- osis due to Nocardia brasiliensis or Nocardia caviae may occur following local trauma with inoculation of the organism. This may present as cellulitis, pyoderma, abscesses, or lymphocu- taneous sporotrichoid lesions. The treatment of cutaneous sporotrichosis is with oral potassium iodide. M. marinum often responds to rifampin and ethambutol or minocycline. Nocardiosis is conveniently and effectively treated with sulfa- methoxazole-trimethoprim.

The diagnosis of ulceronodular infections of the skin requires a careful epidemiological, oc- cupational, and avocational history. For exam- ple, blastomycosis is endemic in North America along the Mississippi and Ohio river basins, along the St. Lawrence river valley, and in the states and provinces bordering the Great Lakes. Cutaneous disease is the most common extra- pulmonary manifestation of blastomycosis, oc- curring with or without concurrent active pul-

FIG. 5. Skin ulcer-loss of epidermal and dermal layers.

Page 9: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

monary disease in 40 to 80% of cases. Infection characteristic of actinomycetes. Nocardia spe- due to S. schenckii or Nocardia species is most cies are weakly acid-fast. In sporotrichosis, or- often associated with traumatic inoculation from ganisms are infrequently seen, but occasionally a soil or plant source, whereas M. marinum round, oval, or cigar-shaped yeast cells, 3 to 8 infection is associated with swimming pool or pm in size, may be seen with periodic acid- aquarium contact. Anthrax and tularemia are Schiff or Gomori-methanamine-silver stain. If zoonoses, and a history of contact with the there is a history of swimming pool or aquarium appropriate animal vector should be sought. contact, a Ziehl-Neelsen or fluorochrome stain

Preexisting cutaneous ulcers may also become for mycobacteria should be done. The skin le- secondarily infected. Ischemic, diabetic, and sion aspirate or biopsy should be cultured aero- decubitus ulcers are often colonized and occa- bically on blood agar at 35 to 37°C and on sionally infected with a variety of bacteria. In- Sabouraud dextrose medium at room tempera- fection may become apparent with purulent ture. These media will support the growth of S. drainage, surrounding inflammation, underlying schenckii and Nocardia species, but as growth abscesses, osteomyelitis, or bacteremia. Infec- of these organisms is slow (2 to 7 days), the tions are typically mixed with aerobic gram- plates should be kept for at least 4 weeks before negative bacilli, streptococcal species, and anae- being discarded as negative. Sabouraud medium robes. supplemented with chloramphenicol and cyclo-

Laboratory heximide may also be used to reduce contami- nation with commensal flora but may not sup-

Unfortunately, there is often a poor correla- port the growth of Nocardia species. Nocardia tion between organisms isolated from superficial species may also be grown on mycobacterial ulcer swabs compared with those recovered culture media. Biopsy specimens for the recov- from deep tissue (33, 34). Therefore, the most ery of M. marinum should be homogenized or reliable specimens are obtained by curettage of ground in sterile saline and inoculated directly the base of the ulcer following the removal of (without decontamination) onto routine media overlying debris or by surgical biopsy of deep for the isolation of mycobacteria, incubated at tissues without contact with superficial layers of 30 to 32 and 35 to 37°C (38). Also broth, such as the ulcer (32, 33). Middlebrook 7H9 or 7H12, which is used in

In general, exudate from an ulcer or biopsy of Bactec 460 (Johnston Laboratories), may be a nodular lesion should be routinely examined used as long as it is incubated at 30 and 35°C. by Gram stain and cultured aerobically on blood The diagnosis of tularemia is best made by agar and MacConkey agar. Sabouraud dextrose detecting a fourfold rise in antibody titer during medium and Sabouraud medium supplemented a 2- to 3-week period of illness or by noting a with chloramphenicol and cycloheximide may titer of 2 1: 160 after a 2-week illness. No attempt be used if fungal infection is considered likely. If should be made to isolate the organism except in diphtheria is suspected, tellurite blood agar may specialized laboratories in view of the risk of also be used. laboratory-acquired infection in the staff.

The sporotrichoid lesions produced by S. schenckii, M. marinum, and Nocardia species SINUS TRACTS

are clinically indistinguishable. The etiological The causative organisms and laboratory meth- diagnosis is made by histological examination ods associated with infections in which a sinus and culture of purulent exudate, aspirate, or tract develops are listed in Table 3. A sinus tract biopsy of skin lesions. Histologically, stainable is a communication between an infected deep organisms may be sparsely distributed, but if tissue or abscess through subcutaneous tissue infection is due to Nocardia species, a Gram and opening onto the skin surface (Fig. 6). These stain may reveal branching, gram-positive bacilli arise from deep infections such as osteomyelitis,

CUMITECH 23 SKIN AND SUBCUTANEOUS TISSUE INFECTIONS 7

TABLE 3. Sinus tracts

Diseases and syndromes Common causative organisms Laboratory diagnostic methods

Actinomycosis

Madura foot

Tuberculosis

Miscellaneous deep or chronic foci of infection

Actinomyces species

Petriellidium boydii, Madurella myce toma tis, Phialophora verrucosa

Mycobacterium tuberculosis

s. aureus, Enterobacteriaceae, Pseudomonas spp.

Gram stain, anaerobic culture in blood agar and in a broth for 1 to 2 weeks

KOH, culture on Sabouraud with and without chloramphenicol and cycloheximide

Fluorochrome, Ziehl-Neelsen smear, culture on Lowenstein-Jensen medium

Gram stain, culture aspirate or deep tissue on blood agar, MacConkey agar

Page 10: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

8 SIMOR ET AL.

Epidermis

3

1 -

Dermis

Subcutaneous

Fascia

MUSCl9

Osteomyelitis

Bone

fat

FIG. 6. Sinus tract from chronic osteomyelitis.

pyomyositis, lymphadenitis, or in&a-abdominal abscesses. In many instances the infection is polymicrobial and the organisms colonizing the cutaneous portions of the tract may be different from those deep in the tissues. For this reason cultures taken from the cutaneous exit of the sinus tract may be misleading.

Several specific organisms are characterized by soft tissue infections with sinus tracts. S. aureus produces deep abscesses and carbuncles discharging thick pus. Cervical lymphadenitis from mycobacteria, especially tuberculosis in the neck, may produce the chronic draining sinuses known as scrofula. Actinomycosis, clas- sically defined as lumpy jaw, is an extremely painful hard swelling around the angle of the jaw that spontaneously drains watery secretions containing “sulfur granules.” These yellow granules are composed of microbial clumps. If left untreated, actinomycosis progresses to a chronic draining sinus. The source of the orga- nism is the patient’s oral cavity, and poor dental hygiene may be an etiological factor. Madura foot occurs when soil organisms, such as Nocar- dia species and various fungi (e.g., Petriellidium boydii, Madurella mycetomatis, and Phialo- phora verrucosa), are inoculated into the soft tissues of the foot to produce multiple abscesses with sinus tracts and sometimes osteomyelitis.

Laboratory The culture of sinus tracts is extremely dif&

cult in that reliable specimens are difficult to obtain. There is a poor correlation between the results of culture of superficial material and that obtained from deeper infected tissues. If surgical exploration is performed, then culture should be taken from the deepest portion of the sinus tract possible. If generalized symptoms such as fever and chills are present, then blood cultures may reveal the more significant organisms. Occasion- ally a deep abscess or portion of the tract can be aspirated, allowing for a more reliable specimen.

CUMITECH 23

Culture procedures should be the same as those for a surgical wound (see below) and should be designed to recover both facultative and anaer- obic bacteria. Granules found in cases of myce- toma should be cultured. The lack of reliability of culturing superficial drainage material will jus- tify a surgical procedure to obtain a good speci- men in those circumstances where the severity demands an accurate microbiological diagnosis.

BURN CULTURES

Burn injuries may be classified according to the responsible agent, such as flame, scald, chemical, and electrical. Although this may be important in recognizing and managing the com- plications associated with each type, the major concerns are the total area and depth of the burn. The depth is used to distinguish among first-, second-, and third-degree burns. First- degree burns are superficial and require little treatment. Second-degree burns may show blis- tering and loss of surface epithelium but eventu- ally heal without scarring or grafting. A third- degree burn is a full-thickness skin injury and results in permanent loss of the skin and replace- ment with scar tissue unless grafted. The sever- ity of the burn is expressed as the estimated percentage of the body surface that has suffered second- and third-degree burns. When the sec- ond- and third-degree burns total greater than 10% of the body surface in children and 15% of the body surface in adults, the patient is admit- ted to a hospital. Other factors such as smoke inhalation and the site of the burn may result in admission of patients with lesser areas burned.

The greatest danger to the patient during the initial therapy is fluid and electrolyte imbalance due to excessive loss through the burned tissue. Modem therapy has greatly increased the sur- vival of patients during this stage, and sepsis is now the most common cause of death. Histori- cally, hemolytic streptococci and staphylococci were the commonest organisms encountered (23). With the advent of potent antimicrobial agents, these are more readily prevented or controlled, and methicillin-resistant S. aureus, the gram-negative bacilli, notably P. aerugin- osa, and yeasts such as C. albicans or filamen- tous fungi such as Fusarium sp. have become the predominant organisms (23). Attempts to prevent infections have included systemic and topical antimicrobial agents as well as protective isolation techniques. Early removal of eschar (burned tissue) and grafting also help to prevent infection while reducing the complications asso- ciated with scarring.

Laboratory Many studies during the 1960s developed the

following concept of the sequence of events in

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CUMITECH 23 SKIN AND SUBCUTANEOUS TISSUE INFECTIONS 9

burn sepsis (3, 5, 8, 13, 20, 22, 39). The surface of the burn contains dead tissue and protein-rich fluid from the patient. Organisms from the pa- tient or the environment colonize this surface. Growth on the surface continues until a heavy microbial load is present. When a large enough concentration is present, extension into the un- derlying tissues occurs and generalized infection with bacteremia ensues. The studies suggest that the occurrence of invasion with complications is associated with bacterial counts of ~10~ CFUlg of tissue. This led to the development of quan- titative methods, both smears and cultures, for assessing surgically removed biopsies of burns. It has been demonstrated that surface cultures alone are inadequate and often misleading. Con- sequently, the culture of deeper tissues is used in many laboratories, a procedure that is also controversial because of difficulty in interpreta- tion.

Although biopsies have been widely used, certain inadequacies have been noted. Burns are not evenly colonized and the selection of the site of biopsy is important. Lists of factors to be considered in choosing a biopsy site have been published to guide surgeons (28). Marked varia- tions within the biopsy itself have also been documented by Woolfrey et al. (43), who di- vided biopsies in half and treated each part as a separate biopsy. Correlation between the two halves is poor, suggesting marked variations within the tissue. Another major concern is the inability to estimate the depth of microbial inva- sion into the tissue regardless of the method used. This has led to a variety of techniques to estimate the depth to which organisms have spread. These methods have included a variety of histopathological and culture techniques.

(i) Quantitative smear and culture. Quantita- tive smear and culture are performed on a sur- gically excised biopsy of the burn. While it is desirable to obtain a generous portion of tissue, such as 0.5 g, usually one has to accept a smaller amount. An area suggestive of infection is cho- sen, and a portion of the tissue down to and including viable bleeding tissue is removed and submitted to the laboratory in a sterile con- tainer. In the laboratory the biopsy is weighed, utilizing a scale with an accuracy of +O.OOl g. The tissue is then homogenized with either a hand grinder or an electric homogenizer in a measured amount of broth or saline. The result- ing homogenate is further diluted to produce a range of 10-l to 10B5 (wt/vol) dilutions. With either a loop or a pipette measured volumes are then placed on a variety of agar plates, usually including sheep blood agar and MacConkey agar. Anaerobic cultures are not routinely done by most laboratories as anaerobic infections are uncommon complications. Identification and

susceptibility testing are performed on the iso- lates, and the quantitative value of each isolate is calculated from the weight of the biopsy and the dilution.

Example: Biopsy weight and dilution = 0.2 g of tissue homogenized in 2 ml of broth (a)

l:lO, l:lOO, 1:1,0(H) dilutions made

Homogenate; all dilutions plated, using a O.OOl-ml quantitative loop (b)

Result- Homogenate = >lOO colonies of Esche-

richia coli 1:lO dilution (c) = ~80 colonies of E. coli 1: 100 dilution = 1 colony of E. coli 1: 1,000 dilution = no growth

Calculation

colony count x dilution (a x b x c)/weight of biopsy (g) = CFU/g of tissue

(80 x [lo (a) x 1,000 (b) X 10 (c)1)/0.2 g = 4 x 10’ CFU/g of tissue

Methods for testing susceptibility to topical agents have been developed but are not rou- tinely used as they lack standardization and the clinical significance remains uncertain.

Quantitative smears may also be prepared at the same time by the method reported by Magee et al. (24). A measured amount of homogenate is spread evenly over a l-cm2 area of a slide and allowed to dry. A Gram srain is performed, and 10 fields are examined with a 100x oil immersion lens. A series of calculations allows the deter- mination of the bacterial counts in terms of organisms per gram of tissue.

(ii) Histopathological techniques. Histopatho- logical techniques have been used to detect fungal infection and in an attempt to determine the location of organisms in burned tissue. The standard surgical pathology techniques of frozen section and quick section have been applied. However, technical problems may be encoun- tered in obtaining good sections, especially when the frozen section method is used. The biopsies are usually graded by the classification of Pruitt and Foley (29). In this classification the grades extend from grade 1 (surface organisms only) to grade 6 (invasion of viable tissue). The histopathological methods have a number of disadvantages. The amount of tissue examined is very small, being limited to a few thin slices taken from the biopsy. Recognition of organisms in tissue sections is more difficult than smears and depends on the quality of the slide, stains used, and experience of the microscopist. The concentration of bacteria required to allow de-

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10 SIMOR ET AL.

TABLE 4. Wound infections

CUMITECH 23

Diseases and syndromes Common causative organisms Laboratory diagnostic methods

Simple postoperative wound infection

Complicated wound infection

S. aureus, S. epidermidis, group A streptococci, Enterobacteriaceae, Enterococcus spp., Bacteroides spp., Clos tridium spp.

Group A streptococci, S. aureus, Enterobacteriaceae, Pseudomonas spp., A. hydrophila, V. vulnljkus, Bacteroides spp., Clostridium spp., anaerobic cocci, microaerophilic cocci, Fusobacterium spp.

Gram stain; culture of pus, aspirate, or tissue on blood agar and MacConkey aerobically; anaerobic methods as in Cumitech 5 ; Trypticase soy broth

Gram stain; aerobic, microaerophilic, and anaerobic culture of pus or tissue (see Cumitech 5)

tection has not been determined although expe- rience has shown that organisms are readily detected in biopsies with lo5 CFU or more per g of tissue when quantitative counts have been performed on the same biopsy specimen. Histo- pathological methods require simultaneous cul- ture to provide the identification and antimicro- bial susceptibilities of the organisms. Although the correlation between the methods is usually good, some cases will demonstrate discrepan- cies between histology and microbiological as- sessment, making the correlation difficult or unreliable.

(iii) Miscellaneous culture methods. Surface culture techniques have been investigated with swabs, contact plates, and contact sponges. However, these are not recommended because they give no estimation of penetration and fail to correlate with clinical experience. Levine et al. (22) reported a simple quantitative swab culture technique involving traumatizing the burn sur- face with the swab and placing it in transport medium for quantitative culture. Neal et al. (27) cultured frozen section slices of burn biopsies on agar. By observing the location of colonies in relationship to the tissue structures, an estimate of invasiveness can be made and graded. The grades ranged from stage I (no growth in 16 h) to stage III (full-thickness growth). Recently a technique consisting of an impression or touch preparation of the deep aspect of a burn biopsy and a swab culture from the depths of the biopsy site has been described (2). In practice this has proved as useful as and less expensive than quantitative smear and culture. All of these culture techniques have been described as useful and valuable. At present no commonly accepted standard method exists.

Quantitative smear and culture have been the most commonly used techniques in the past. Some bum centers have accepted other methods because they believed them to be superior to smear and culture. To be useful, methods must cause a minimum of patient discomfort, give rapid results, be inexpensive and accurate, esti-

mate the depth of invasion, allow the identifica- tion and antimicrobial susceptibility testing of the organisms, and correlate well with clinical findings. None of the present techniques satisfy all of these requirements.

SIMPLE POSTOPERATIVE WOUND INFECTIONS

The organisms associated with simple and complicated wound infections are listed in Table 4. Infection in a surgical wound occurs when the wound, usually in the intraoperative or immedi- ate postoperative period, is contaminated by microorganisms. The sources of the organisms may include colonized body sites of the patients, such as the nose, oral cavity, female genital tract, alimentary tract, and skin (25). The med- ical and nursing stti may also be a source of organisms, as may the inanimate hospital envi- ronment. Host factors that may contribute to the pathogenesis of a surgical wound infection in- clude obesity, diabetes, vascular insufficiency, and immune suppression. Microbial factors in- clude microbial load and “virulence” of the organism. Surgical factors, such as the duration of an operation, poor hemostasis, the presence of a foreign body, and devitalized tissue, may contribute to the likelihood of infection. In the presence of these risk factors the inoculum size necessary to initiate infection is much smaller than that required to cause infection in the healthy tissue (9).

Infection rates vary from one type of surgical procedure to another. Surgical procedures may be classified as clean, clean-contaminated, con- taminated, and dirty (6, 7). Implicit in this clas- sification is the risk of postoperative infection. Additionally, infections of a remote site, for example, a urinary tract infection, place the surgical patient at a higher risk of postoperative infection. Overall, infection rates in modern practice range from 1 to 5%. The principal patho- gens are S. aureus, Staphylococcus epidermidis, E. coli, Klebsiella spp., Enterobacter spp., Pseu- domonas spp., Enterococcus spp., Bacteroides

Page 13: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

CUMITECH 23 SKIN AND SUBCUTANEOUS TISSUE INFECTIONS 11

spp., and Clostridium spp. Some wounds that appear infected may not yield a pathogen on culture while others will grow multiple species.

Superficial wound infections often start at a suture and may be painful, tender, red, and swollen. Pus may exude, particularly if one or more sutures are removed to allow free drain- age. Malodorous discharge may suggest the presence of anaerobic bacteria.

Mycobacterium chelonei and Mycobacterium fortuitum’ may cause infection, complicating car- diac surgery, mammoplasty , and ocular and other clean surgery (41). These organisms may produce chronic disfiguring disease.

Antimicrobial management must be tailored to the bacteriological diagnosis. Empiric therapy will usually include broad-spectrum agents with activity against gram-positive cocci (e.g., a first- generation cephalosporin), as well as one with activity against gram-negative bacteria (e.g., an aminoglycoside). If anaerobes are suspected, one may choose clindamycin, cefoxitin, or me- tronidazole, all effective against Bacteroides spp., the common pathogens. Penicillin G is the drug of choice against Clostridium perfringens.

Laboratory A volume of aspirated pus or a swab heavily

impregnated with pus may be examined micro- biologically. A Gram-stained smear may give some indication of the variety of infecting flora. Some laboratories make it a practice to culture exudates from superficial wounds for aerobic and facultative organisms on blood agar and MacConkey agar, as well as to prepare a broth culture. Culture of superficial wounds for anae- robes in the absence of a clinical indication is expensive and unrewarding. Pus from deep wounds or from wounds showing gas bubbles or foul-smelling discharge should be cultured for anaerobes as well as aerobic and facultative bacteria. Details of specimen collection and processing for anaerobes are presented in Cumi- tech 5 (11).

M. chelonei and M. fortuitum, although classed as rapid-growing mycobacteria capable of growth on sample media, usually require 1 to 6 weeks to grow on primary culture. In routine diagnostic laboratories such infections may be missed, unless one is aware of their possible role and cultures are saved. These organisms, espe- cially M. chelonei, may be misidentified as diph- theroids in a broth culture unless an acid-fast stain is performed.

When isolates from infected wounds are re- ported, it is essential to take into account the source of the specimen. Thus, all coagulase- negative staphylococcal isolates from infected sternotomy wounds or associated with vascular or implant orthopedic surgery should be consid-

ered as potential pathogens and antimicrobial susceptibility tests should be carried out. Con- versely, low numbers of coagulase-negative staphylococci associated with enteric flora in an infected colon resection wound could be disre- garded to the extent that susceptibility testing need not be performed. The reason for this is that they do not constitute a clinical problem and will disappear when the other pathogens are eliminated.

COMPLICATED WOUND INFECTIONS Complicated infections of the skin and subja-

cent structures may occur following surgery or trauma. Classification of these infections is dif- ficult due to overlapping of affected anatomical sites, causative organisms, and clinical manifes- tation. Many of these infections are severe, rapidly progressive, and associated with a high mortality rate.

Infectious gangrene is a rare disease in which bullous necrosis of the skin may be associated with bacteremia and metastatic lesions. This disease is often fatal.

Synergistic gangrene (Fig. 7), sometimes re- ferred to as Meleney’s gangrene, usually com- plicates surgery of the alimentary tract. It starts as an ulcer near the wound and can spread to affect much of the anterior abdominal wall.

Gas gangrene is usually associated with C. perfringens, an organism that may colonize a wound without causing disease, may cause a spreading cellulitis, or may extend into muscle to cause myonecrosis. It may be associated with a thin watery discharge rather than a purulent exudate. A similar syndrome of muscle necrosis may be caused by Aeromonas hydrophila and Vibrio vulnijkus, and cellulitis may be caused by Vibrio species, Klebsiella spp., E. coli, and/or nonclostridial anaerobes such as Bacteroides spp. and cocci.

Necrotizing fasciitis (Fig. 8) usually starts at an abdominal surgical wound and spreads later- ally to the flanks, up to the nipple line, and down to the inguinal region. The patient is usually very ill. The overlying skin appears normal early in the illness, turning reddish-blue as the disease

FIG. 7. Progressive bacterial synergistic gangrene.

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12 SIMOR ET AL. CUMITECH 23

Other antimicrobial agents directed at faculta- tive and aerobic bacteria may include imipenem, ceftazidime, ciprofloxacin, - and combinations containing beta-lactamase inhibitors such as cla- vulanic acid and sulbactam. Antimicrobial ther- apy directed against anaerobes is essential. This may include metronidazole, clindamycin, pipe- racillin , and cefoxitin.

Laboratory

FIG. 8. Necrotizing fasciitis .

progresses. Bus may drain through the skin in the flanks or in other parts remote from the original wound.

Foumier’s disease (Fig. 9) is a form of necro- tizing fasciitis affecting the perineum and scro- tum in which the superficial layers of the skin blacken and slough off. Anaerobic bacteria such as Bacteroides spp., Fusobacterium spp., Clo- stridium spp., and gram-positive cocci, as well as facultative bacteria such as members of the Enterobacteriaceae, staphylococci, and entero- cocci, may be involved. Microaerophilic strep- tococci are often seen in synergistic gangrene, often in association with S. aureus and members of the Enterobacteriaceae. Some clinicians (lumpers rather than splitters) like to reduce these myriad descriptions to three syndromes: (i) crepitant cellulitis, which may be clostridial or nonclostridial; (ii) necrotizing fasciitis, in- cluding Meleney’s gangrene and Foumier’s dis- ease; and (iii) gas gangrene with myonecrosis.

Infection may become complicated and ex- tend to the muscles of the leg when the arterial supply is compromised, as in diabetes mellitus. There may be extensive myonecrosis caused by anaerobes such as Clostridium spp., anaerobic cocci, and Bacteroides spp. in the area of vas- cular insufficiency. Facultative flora may also be

The bacteria commonly isolated from wound infections include S. aureus, group A strepto- cocci, anaerobic cocci, Clostridium spp., espe- cially C. perfringens, members of the Entero- bacteriaceae, Bacteroides spp., and Fusobac- terium spp.

Effective laboratory investigation requires the collection of a volume (up to 5 ml) of aspirated pus or excised tissue. Fluid specimens may be transported in anaerobic transport tubes or vi- als, anaerobic biobags, or if these are unavail- able, plugged syringes or gassed out tubes. Tis- sue samples may be sent to the laboratory in dry sterile test tubes or in gassed out tubes.

Gram-stained smears may indicate the variety of microorganisms associated with the lesion, and presumptive therapy can be guided by the Gram stain results. This is particularly the case with C. perfringens myonecrosis, which may be rapidly progressive and which may be recog- nized on the basis of brick-shaped gram-positive rods. Note that on Gram-stained smears these may decolorize readily and some organisms ap- pear gram negative. There are few pus cells in C. perfiingens infection. Specimens should be cul- tured on blood agar and on a selective medium such as MacConkey agar. The common faculta- tive and aerobic flora will appear within 24 h. The microbiological examination of all of these infections requires culturing for anaerobes (11)) as well as aerobes and facultative anaerobes.

present, including Proteus spp. The treatment of these infections is surgical INFECTIONS COMPLICATING BITES

with adjunctive antimicrobial therapy (17, 26, Both human and animal bite wounds may be 37). Since the large majority involve a mixed contaminated with oral flora, as may those infecting flora, including facultative anaerobes caused by trauma related to the mouth, such as and anaerobes, a broad-spectrum antimicrobial fist injuries from striking teeth, and those asso- therapy is indicated. This may consist of an ciated with dental injuries or procedures (Table aminoglycoside with clindamycin or a beta- 5). lactam effective against gram-positive cocci. Bite-associated infections vary according to

the depth of the bite, the dental pattern of the mouth, and the oral flora present. They also vary to some degree with the site of the injury as infection tends to spread along fascial planes. Human bites or fist injuries are always contam- inated with oral flora and tend to cause severe necrotizing infections unless treated aggres- sively. Dog and cat bites are often deep puncture wounds and are sometimes infected by orga-

FIG. 9. Fournier’s gangrene. nisms absent or infrequent in human bites. Her-

Page 15: Cumitech 23: Infections of the Skin and Subcutaneous Tissues

CUMITECH 23 SKIN AND SUBCUTANEOUS TISSUE INFECTIONS

TABLE 5. Bites

13

Diseases and syndromes Common causative organisms Laboratory diagnostic methods

Animal bites

Cat scratch disease Human bites

P. multocida, DF-2, S. moniliformis, S. minor

Unknown Normal oral flora

Gram stain; blood agar; MacConkey agar; blood culture

Histology Gram stain; culture aerobically on blood

agar, chocolate agar, and MacConkey agar; culture anaerobically as described in Cumitech 5

bivorous animals such as horses and cows have a bite that includes a grinding action, resulting in severe tissue maceration.

Rabies and tetanus are infectious complica- tions of bites but are not investigated by wound culture. Culture of the fresh bite is not rewarding and simply reflects the oral flora of the biter. Cultures of infections resulting from bites nearly always yield a mixture of organisms, including anaerobes. A common isolate from animal bites is Pasteurella multocida. This is part of the oral flora of cats and dogs, as well as other animals ranging from rabbits to lions. Bacteremia arising from animal bites may yield unusual isolates. Bacteremia with the organism DF-2 (dysgonic fermenter type 2) has been associated with dog and cat bites (1,4, 36). Bacteremia as part of rat bite fever caused by either Streptobacillus mo- niliformis or Spirillum minor is associated with rodent bites. The latter organism is difficult to culture, requiring animal inoculation to detect the bacteremia. Another unusual infection asso- ciated with pet bites and cat scratches is cat scratch disease. Infection at the site of initial injury is followed by the enlargement of the local lymph nodes as evidence of a suppurative lym- phadenitis. Gram-negative bacilli have been demonstrated in tissue sections of the lymph nodes, and a recent report suggests that vegeta- tive bacteria have been isolated in artificial cul- ture media-biphasic brain heart infusion agar and broth (10). The important principles in treat- ing bites of any type are adequate debridement of dead tissue and adequate drainage by leaving the wound open. Prophylactic antibiotics are recommended as these wounds are always con- taminated.

Laboratory

Cultures of fresh animal bites are not war- ranted as they yield no useful clinical informa- tion. The best material for culture is usually pus aspirated from the depths of the wound or cul- tures taken during the time of incision and drainage or debridement of the infected wound. Both aerobic and anaerobic cultures should be performed with a variety of media to help sepa- rate the anticipated mixture of organisms.

1.

2.

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4.

5.

6.

7.

8.

9.

10.

11.

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17.

18.

19.

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