Facial cellulitis pdf

However, it is a good idea to seek medical attention immediately. The medical specialist is likely to conduct a physical exam after checking the medical history of the patient.

Certain laboratory tests that are conducted can confirm the presence of facial cellulitis. Treatment is decided by culturing the bacteria that is causing the infection. Facial cellulitis is commonly treated with antibiotics for a period of 10 to 14 days.

If the infection is accompanied by high fever, hospitalization may be suggested by the doctor. Severe cases may require intravenous administration of antibiotics. Most patients who present with a condition of facial cellulitis have a recurrence of the infection.

Here the treatment course is usually longer to completely eradicate the infection. Surgery may be required in extreme cases to drain the pus when the patient develops an abscess on the face.

Dead infected tissue is sometimes derided surgically to ease the healing of the surrounding skin. The accompanying pain and fever are treated with over-the-counter drugs.

Control of predisposing conditions helps to prevent the risk of infection in the first place and its recurrence. These may include: glycemic control, weight control, avoiding injury to the skin as far as possible, wearing appropriate protective gear when playing outdoor sports, avoiding swimming with broken facial skin, keeping cuts and bruises clean by washing frequently. Severe cases of facial cellulitis may take a long time to get completely cured.

Strong antibiotics are also known to reduce the defense system of the body. Sixty days of treatment is recommended when associated with bioterrorism as concomitant inhalation may have occurred. Until susceptibilities are available, ciprofloxacin is rational empiric therapy for bioterrorism-related cases.

Other fluoroquinolones such as levofloxacin, gatifloxacin, or moxifloxacin are also likely to be effective. Initiation of intravenous vs oral therapy depends upon the severity of the illness, particularly the degree of edema. Some have suggested systemic corticosteroids for patients who develop malignant edema, especially of the head and neck, but studies supporting this recommendation are lacking.

Airway compromise requiring intubation or tracheostomy may occur with malignant edema. In classic cat scratch disease, a papule or pustule develops from 3—30 days following a scratch or a bite. Lymph nodes that drain the infected area enlarge about 3 weeks after inoculation.

The disease course varies, but lymphadenopathy generally resolves within 1—6 months. Bartonella henselae causes most cases of cat scratch disease in immunocompetent hosts.

Bacillary angiomatosis, seen in immunocompromised patients, especially with AIDS, can occur from either B. Diagnosis of Bartonella infections may be difficult because the organism is fastidious and difficult to grow in culture. Serological testing supports the diagnosis, although there is cross-reactivity between B. PCR is a diagnostic option.

A positive Warthin-Starry silver stain of infected lymph node tissue is useful to confirm the diagnosis, although it cannot differentiate species of Bartonella.

Treatment of cat scratch disease with antimicrobial agents has had variable, but rarely dramatic, results. A single, double-blind placebo-controlled study involved 29 patients, 14 of whom received azithromycin []. Cutaneous bacillary angiomatosis therapy has not been systematically examined. Based on case reports and small series, either erythromycin mg qid or doxycycline mg bid appears effective []. The duration of initial therapy, while not standardized, should be for 2 weeks to 2 months.

With relapses, retreatment with prolonged therapy months should be entertained until immunocompetence returns. HIV-infected patients may require lifelong treatment []. Erysipeloid is a cutaneous infection caused by Erysipelothrix rhusiopathiae a thin, pleomorphic, non-spore-forming gram-positive rod.

It is a zoonosis acquired by handling fish, marine animals, swine, or poultry. One day to 7 days after exposure, a red maculopapular lesion develops, usually on fingers or hands. Erythema spreads centrifugally, with central clearing. A blue ring with a peripheral red halo may appear, giving the lesion a target appearance. A severe generalized cutaneous variety also occurs.

Systemic symptoms and leukocytosis are unusual. Untreated erysipeloid resolves over about 3—4 weeks, but treatment probably hastens healing and may reduce systemic complications. Based on in vitro susceptibilities and anecdotal experiences, penicillin is appropriate.

Cephalosporins, clindamycin, or fluoroquinolones should be effective for those intolerant of penicillin. Erysipelothrix rhusiopathiae is resistant to vancomycin, teicoplanin, and daptomycin [, , , ]. Glanders, characterized by ulcerating nodular lesions of the skin and mucous membrane, is caused by the aerobic gram-negative rod Burkholderia mallei. Glanders is mainly a disease mainly of solipeds eg, horses and mules. Humans become accidental hosts either by inhalation or skin contact.

Although other organs may be involved, pustular skin lesions and lymphadenopathy with suppurative nodes can be a prominent feature. Optimal therapy of glanders is poorly defined. The organism is susceptible to ceftazidime, gentamicin, imipenem, doxycycline, and ciprofloxacin []. A recent laboratory-acquired case was successfully treated with imipenem and doxycycline for 2 weeks, followed by azithromycin and doxycycline for an additional 6 months [].

Plague results from infection with Yersinia pestis , a facultative anaerobic gram-negative coccobacillus. It primarily affects rodents, being maintained in nature by several species of fleas that feed on them.

Three plague syndromes occur in humans: septicemic, pneumonic, and bubonic. Bubonic plague, the most common and classic form, develops when humans are bitten by infected fleas or have a breach in the skin when handling infected animals. Domestic cat scratches or bites may also transmit bubonic plague. Patients usually develop fever, headache, chills, and tender regional lymphadenopathy 2—6 days after contact with the organism.

A skin lesion at the portal of entry is sometimes present. Patients with bubonic plague may develop septicemia and secondary plague pneumonia, which is transmissible person-to-person. Diagnosis can be made by blood cultures and by aspirating lymph nodes for staining and culture. PCR is available at reference laboratories. Serologic tests may provide retrospective confirmation. No controlled comparative trials of therapy for plague exist.

Gentamicin is a reasonable substitute for streptomycin if the latter is not available, although there is but limited experience with gentamicin in the treatment of plague. Based on in vitro susceptibilities and murine models, fluoroquinolones are another option.

Ciprofloxacin has been suggested as a drug for both treatment and prevention of plague due to biowarfare agents despite a lack of documented efficacy in humans. The optimal duration for treating bubonic plague is unknown, but 10—14 days is probably adequate.

Patients with bubonic plague may develop secondary pneumonic plague and should be placed in respiratory isolation until after 48 hours of effective drug therapy. Francisella tularensis , while hardy and persistent in nature, is a fastidious, aerobic, gram-negative coccobacillus. Illness can often be categorized into several fairly distinct syndromes: ulceroglandular, glandular, typhoidal, pneumonic, and oculoglandular or oropharyngeal.

The glandular varieties are generally acquired by handling infected animals, by tick bites, and sometimes by animal bites, especially cats. Biting flies occasionally transmit the illness in the United States, while mosquitoes are common vectors in Europe. After an incubation period of 3—10 days, the patient typically develops a skin lesion ulcer eschar at the entry site of the organism along with tender adenopathy in regional lymph nodes, hence the name ulceroglandular.

The illness is often associated with substantial fever, chills, headache, and malaise. Confirmation of the diagnosis is usually serological. Routine cultures are often negative unless cysteine-supplemented media are utilized. The laboratory should be notified when tularemia is suspected because of the health risks posed to laboratory personnel. Unsuspected growth of F.

PCR may also be useful for diagnosis. No prospective controlled or randomized trials of therapy for tularemia have been performed, nor has the optimal duration of treatment been established. Streptomycin has been considered the drug of choice for tularemia for several decades [].

Since then, a few patients have been received fluoroquinolones. Acutely ill adults or children should receive an aminoglycoside, preferably streptomycin or possibly gentamicin. Although no data exist, treatment with a parenteral agent until the acute illness is controlled, followed by an oral agent, seems rational for the duration of 7—10 days. Treatment of severe cases should be extended to 14 days. For mild to moderate disease, oral tetracycline mg qid or doxycycline mg bid is appropriate.

A few cases have been treated with fluoroquinolones with mixed results []. Oral levofloxacin mg daily or ciprofloxacin mg bid in adults may be reasonable in mild to moderate illness. For oral regimens, patients should receive at least 14 days of therapy. Despite clinical responses and appropriate treatment in one study from France, Skin and soft tissues are common sites of infection for HIV-negative patients with a compromised immune system, posing a major diagnostic challenge [, ], as the differential diagnosis is broad and includes drug eruption, skin or soft tissue infiltration with the underlying malignancy, chemotherapy- or radiation-induced skin reactions, graft-vs-host disease among allogeneic transplant recipients, Sweet syndrome, erythema multiforme, and leukocytoclastic vasculitis [, ].

Because the intensity and type of immune defect diminishes or alters dermatological findings, cutaneous lesions that appear localized or innocuous may actually be a manifestation of a systemic or potentially life-threatening infection. The differential diagnosis for SSTIs in immunocompromised patients is usually wider than that for immunocompetent patients and often includes bacterial, viral, fungal, and parasitic agents.

Organisms that cause these infections will vary based on the underlying immune defects eg neutropenia, cellular immune defects, iatrogenic related to the use of intravascular catheters , and many of the infecting organisms are not typically considered pathogenic in normal hosts opportunistic organisms such as Aspergillus fumigatus.

However, infectious agents commonly found in immunocompetent patients eg, S. A careful epidemiologic history eg, exposure to raw seafood, pets, and travel should also be obtained in these patients to consider organisms potentially associated with these exposures when appropriate eg, V.

Use of antimicrobial prophylaxis in these patients has shown to ultimately impact the pathogens that will be isolated when infection develops, and this information should be available to the clinician when assessing immunocompromised patients with skin and soft tissue lesions [, ]. After considering the important specific factors concerning the patient's immunocompromised status eg, neutropenia or neutrophil defects, cellular immune defect, presence of intravascular catheters [, ], the gross morphologic characteristics of the skin lesion s should be characterized, the extent of the infection determined eg, localized vs disseminated , and appropriate diagnostic tests undertaken to identify the infecting pathogen.

Although blood cultures, tests for detection of antigens in blood or vesicular fluid, or nucleic acid amplification techniques in body fluids or tissues may be helpful, the most specific method for an expedited diagnosis is biopsy or aspiration of the lesion to obtain material for histological and microbiological evaluation.

The use of newer molecular methods eg, gene amplification and sequencing will likely impact the management algorithms of immunocompromised patients with skin and soft tissue lesions and result in the earlier use of pathogen-directed antimicrobial therapy [, ]. However, sensitivity of these tests can be significantly affected by the use of antifungal drugs, and in the United States their sensitivity has been reported to be lower than in Europe in various populations of immunocompromised patients [].

Empiric antimicrobial therapy should be initiated immediately in these patients on the basis of their underlying disease, primary immune defect, morphology of skin lesions, use of prior antimicrobial prophylaxis, allergy history, and inherent and local profiles of antimicrobial resistance.

The early identification of an etiologic agent in immunocompromised hosts with SSTIs is essential when deciding whether surgical debridement is warranted because microbial resistance makes dogmatic empiric treatment regimens difficult, if not dangerous.

For this reason, skin biopsy material should be obtained by an experienced dermatologist and evaluated in conjunction with a pathologist who is familiar with this patient population. These guidelines are focused on the diagnosis and management of specific patient groups eg, fever and neutropenia, infection in recipients of hematopoietic stem cell transplant , specific infections eg, candidiasis, aspergillosis , and iatrogenic infections eg, intravascular catheter—related infection.

They are based on published clinical trials, descriptive studies, or reports of expert committees, and the clinical experience and opinions of respected authorities. The development of fever during treatment-associated neutropenia is common, but many patients do not have an infectious etiology determined [, ].

Cancer patients with fever and neutropenia can be divided into low- and high-risk groups []. The determination of differences in patient risk of infection and infectious complications levels high risk and low risk during the period of neutropenia has been recognized and further validated since this clinical guideline was last updated [, ]. The MASCC developed and validated a scoring method that formally differentiates between high-risk and low-risk patients [, ].

Disseminated or complex SSTIs are more likely to occur among high-risk patients. Signs and symptoms of inflammation and infection are often diminished or absent in patients with neutropenia. Skin lesions, no matter how small or innocuous in appearance, should be carefully evaluated. Early involvement of an infectious diseases specialist, a surgeon, and a dermatologist familiar with these patients may result in improved outcome. Initial clinical impressions should be supplemented with a systemic approach to enhance the diagnosis and management of infection.

Blood cultures are critical, and at least 2 sets should be obtained. Radiographic imaging should be performed as clinically indicated, but can be helpful to define the extent of SSTIs when patients are neutropenic. The most specific method for evaluating SSTIs is biopsy or aspiration of the lesion s to obtain material for histological, cytological, and microbiological evaluation.

Prospective studies evaluating the yield of skin biopsy or aspiration have not been performed in adult immunocompromised patients, but most clinicians who manage these patients combine blood cultures, serial antigen detection, nucleic acid amplification techniques, radiographic imaging, and a biopsy or aspiration of the abnormal skin or soft tissue lesion in the hope of increasing the recovery of the offending pathogen and directing pathogen-specific antimicrobial therapy.

This determination helps the clinician define the most likely pathogens and to construct the initial empiric treatment. During the initial episode gram-negative bacteria should be primarily targeted by the initial antibiotic regimen because they are associated with high mortality rates. Although gram-positive bacteria are more common, the addition of antibiotics with gram-positive activity including MRSA is not recommended unless physical findings suggestive of inflammation in the skin and soft tissues are present, the patient is hemodynamically unstable, and risk factors for MRSA are present.

For patients with a persistent episode of fever and neutropenia or recurrent episodes, antibiotic-resistant bacterial or fungal pathogens including Candida and molds become more common [—]. Ecthyma gangrenosum is a cutaneous vasculitis caused by invasion of the media and adventitia of the vessel wall by bacteria, which may be visible on histologic stains of biopsy specimens.

Ecthyma gangrenosum frequently begins as painless erythematous papule s that often progress and become painful and necrotic within 24 hours. Ecthyma gangrenosum has classically been reported to occur with Pseudomonas aeruginosa infections, but similar lesions may be caused by other Pseudomonas species, Aeromonas species, Serratia species, S. Necrotizing fasciitis can present alone or concurrently with myonecrosis in the patient with fever and neutropenia.

Rapidly progressive necrotizing SSTIs may initially be clinically subtle in compromised patients, but MRI scans of the involved area may be helpful in defining the depth of infections. In such infections, immediate surgical exploration by a team experienced in the management of these patients and broad-spectrum antibiotic therapy targeted at gram-negative, gram-positive, and anaerobic bacteria are essential.

Gram-positive pathogens are now the most common bacterial organisms isolated from diagnostic cultures obtained from febrile neutropenic patients [, ]. These pathogens in order of decreasing prevalence include coagulase-negative staphylococci, viridans streptococci, enterococci, S. SSTIs associated with these organisms usually begin as a focal area of tender cutaneous erythema, a macular or maculopapular eruption, or a classic cellulitis.

Common infection sites are the groin, axilla, areas of cutaneous disruption eg, vascular catheter or bone marrow aspiration sites , or other skin sites that are moist and frequently abraded. Hematogenous dissemination of gram-positive bacterial organisms to the skin and soft tissue is uncommon except for S.

A toxic shock—like syndrome with associated diffuse erythroderma has been described with bacteremic toxin—producing streptococci. Painful myositis may also occur with S. HSV, varicella zoster virus VZV , and enteroviruses are rare causes of cutaneous manifestations in patients with neutropenia [].

Their presence usually reflects either a disseminated infection, or, in the case of HSV, the autoinoculation of virus from mucosal sites to adjacent or distant cutaneous sites. HSV and VZV in compromised patients may appear as vesicles similar to those in normal hosts, or as isolated or multiple benign-looking papules with a central eschar ecthyma gangrenosum—like lesion. VZV in compromised hosts may present with the traditional unilateral dermatome distribution, but may also appear as discrete or multiple skin lesions in random distribution.

The appropriate antibiotics for patients with suspected or confirmed SSTI initial infection should be broad-spectrum agents administered at the first clinical signs or symptoms of infection []. No single empiric regimen is superior, but all recommended regimens should meet the following criteria: broad-spectrum antimicrobial activity including P. Infections caused by gram-negative bacilli including P. Despite an increased prevalence of gram-positive bacteria, antibiotics specifically aimed against this group of organisms are not required [, ] unless patients exhibit physical findings of SSTI or catheter-associated infection or are hemodynamically unstable [].

For patients in whom vancomycin may not be an option, daptomycin, ceftaroline, or linezolid should be added to the initial empiric regimen. Linezolid, daptomycin, or ceftaroline have activity against MRSA [] and have received FDA approval for the treatment of SSTIs, but have not been comprehensively studied in patients with neutropenia.

The use of linezolid in this patient population has been associated with delayed ANC recovery [, ]. The combination of ciprofloxacin and amoxicillin-clavulanate is the preferred oral antibiotic regimen for low-risk patients [, ].

Levofloxacin has better gram-positive activity than ciprofloxacin, but is less potent than ciprofloxacin against P. Intravenous acyclovir should be added to the empiric antimicrobial regimen of the rare patient who has not been receiving antiviral prophylaxis effective against HSV or VZV, but has developed skin lesions suspected or confirmed to be caused by these viruses.

In patients with persistent unexplained fever of their first episode after 4—7 days or recurrent fever, yeast and molds are the major cause of infection-related morbidity and mortality Table 7 [, , ]. These later infections are most common among high-risk patients with prolonged and profound neutropenia and they should be considered in any patient with neutropenia and skin and soft tissue lesions suggestive of infection.

In addition, MRSA should also be considered if patients are not receiving antimicrobial agents with activity against MRSA eg, vancomycin, linezolid, daptomycin, or ceftaroline [].

Multiple antibiotic-resistant gram-negative bacilli are more commonly being recovered from cultures of blood and soft tissues, and antibiotic modification is necessary when their presence is suspected or documented Table 7 []. In , infections caused by yeast and molds were the major cause of associated morbidity and mortality in patients with prolonged and profound neutropenia [, ]. Diagnosis of fungal infections remains difficult, and benefits from fungal antigen or DNA detection remain inconsistent [, ].

However, recovery of fungi from aspiration or biopsy of skin or deep soft tissues warrants aggressive systemic antifungal therapy. Surgical treatment should be also considered in patients with skin and soft tissue changes caused by angioinvasive molds eg, Mucor , Rhizopus , and Aspergillus. Candida albicans is the most frequently isolated species; however, fluconazole-resistant yeast ie, Candida krusei and Candida glabrata are increasingly common due to the widespread use of azole prophylaxis [].

Superficial cutaneous candidiasis presents as intertrigo, vaginitis, balanitis, perleche, and paronychia [] and rarely causes dissemination. These lesions can appear as discrete pink to red papules 0. Candida skin lesions are usually nontender, but may develop central pallor, or become hemorrhagic if the patient is thrombocytopenic.

Painful myositis can develop as a consequence of hematogenous infection and is most common with Candida tropicalis [, ]. Muscle and soft tissue abscess formation is uncommon, but when identified it has usually occurred following marrow recovery. Trichosporon beigelii is an uncommon but frequently fatal disseminated fungal infection that often involves the skin [].

Dermatologic manifestations vary from multiple erythematous macules to maculopapular lesions. Biopsy often reveals a mixture of true hyphae, pseudohyphae, budding yeast, and arthroconidia that may be easily mistaken for Candida species.

Cutaneous mold infections are unusual, but there could be local infections at sites of IV catheter insertion or at nail bed and cuticle junctions on fingers and toes, or secondary to hematogenous dissemination [].

Aspergillus , Rhizopus , and Mucor species cause painful erythematous skin nodules that become necrotic and can resemble ecthyma gangrenosum because of their tendency for angioinvasion []. Isolation of Aspergillus from blood cultures is rare, but dissemination is commonly detected at autopsy []. Local Mucor infections have occurred as a consequence of contaminated bandages or other skin trauma, but patients with pulmonary Mucor infection may also develop secondary cutaneous involvement from presumed hematogenous dissemination [, ].

Fusarium species are frequently identified as the infecting pathogen among patients with prolonged and profound neutropenia []. Patients commonly present with myalgias and persistent fever despite antimicrobial therapy. The lesions frequently may have a ring of erythema surrounding an area of central necrosis. Lesions localize preferentially to the extremities, especially the feet, but may also be found on the face and trunk.

Mortality from this infection remains high, although new azole antifungal agents appear promising []. Patients with lymphoma or acute or chronic lymphocytic leukemia, recipients of hematopoietic stem cell transplant HSCT or solid organ transplant SOT , patients receiving corticosteroids and other immunosuppressive drugs eg, monoclonal antibodies, anti-TNF drugs , and patients with primary cellular immunodeficiencies are predisposed to infection.

These patients are at increased risk for infection caused by a select group of bacteria, fungi, viruses, protozoa, and helminths, and some of these pathogens have the capacity to cause SSTIs. Infection should always be high in the differential of a skin lesion or skin lesions in patients with cellular immunodeficiency.

These patients may not have systemic manifestations of infection, and the initial dermatological presentation may be atypical or misleading. Thus clinicians should have a very low threshold to obtain a skin biopsy Table 6. Although most infections occur after primary inoculation at sites of skin disruption or trauma, hematogenous dissemination does occur. The most common manifestations of nontuberculous mycobacteria NTM infection in SOT recipients include cutaneous and pleuropulmonary disease, and, in HSCT recipients, catheter-related infection and bacteremia [].

Disseminated infection with Mycobacterium avium complex occurs preferentially among patients with HIV disease, whereas bloodstream and cutaneous infections with Mycobacterium fortuitum , Mycobacterium chelonae , Mycobacterium abscessus , Mycobacterium ulcerans , Mycobacterium kansasii , Mycobacterium haemophilum , Mycobacterium marinum , or Mycobacterium mucogenicum are more frequent among non-HIV-immunocompromised hosts [].

Dermatologic manifestations include a poorly resolving cellulitis, painless 1- to 2-cm nodules, necrotic ulcers, and subcutaneous abscesses. Treatment of NTM infections of the skin and soft tissues requires prolonged combination therapy duration, 6—12 weeks that should consist of a macrolide antibiotic eg, clarithromycin and a second agent to which the isolate is susceptible.

Surgical debridement is crucial for cultures and sensitivities and in addition is necessary to remove devitalized tissue and to promote skin and soft tissue healing. Definitive guidelines for treatment of these entities have been published [].

Cutaneous Nocardia infections usually represent metastatic foci of infection that have originated from a primary pulmonary source [].

Nocardia farcinica , Nocardia brasiliensis , and other Nocardia species have been associated with cutaneous disease. The dermatologic manifestations are usually limited to subcutaneous nodules or abscesses and panniculitis. Soft tissue abscesses are frequently painless and are described as being cold to the touch. SMX-TMP remains the treatment of choice, but other sulfa antibiotics eg, sulfadiazine and sulfasoxazole , amikacin, imipenem, meropenem, third-generation cephalosporins ceftriaxone and cefotaxime , minocycline, extended-spectrum fluoroquinolones eg, moxifloxacin , linezolid, and dapsone are effective in vitro and in animal models Table 6.

Combination therapy with other agents should be considered in patients with severe infections or profound and lasting immunodeficiency. Prolonged therapy is important, and the duration of treatment 6—24 months should take into account the presence of disseminated disease and the extent of the patient's underlying immunosuppression.

Surgical debridement is recommended for necrotic nodules or large subcutaneous abscesses. Cutaneous mold infections have been increasingly reported in immunocompromised patients with primarily cellular immunodeficiency. Skin lesions can occur as a manifestation of a disseminated disease, a primary cutaneous inoculation, or in the skin site of a previous IV line [, ]. The most common molds causing cutaneous manifestations in these patients include Aspergillus , Mucormycosis , Scedosporium , and Fusarium species [—].

Skin lesions can present as papules, nodules, or ulcers, or with the dermatological appearance of ecthyma gangrenosum. In instances of Aspergillus species, Scedosporium apiospermum , and Fusarium species infections, voriconazole is the best therapeutic option.

Amphotericin B is an excellent alternative. Posaconazole is also a reasonable alternative in combination with amphotericin B or as a transition to oral therapy Table 7.

Cryptococcal infections originate in the lungs, often with early hematogenous dissemination to the meninges and skin or soft tissues, but primary cutaneous cryptococcosis also occurs []. Cutaneous cryptococcal infections may appear as papules often similar to molluscum contagiosum lesions , nodules, pustules, chronic draining necrotic ulcers, or, more subtly, as cellulitis [].

Cutaneous manifestations of acute progressive disseminated histoplasmosis are rare and usually occur in patients with severe cellular immune deficiency [, ]. Skin lesions appear as nonspecific maculopapular eruptions that become hemorrhagic, but oral or cutaneous ulcers are sometimes present, particularly in the subacute, disseminated form of the disease.

Histopathologic analysis of these skin lesions reveals necrosis surrounding the superficial dermal vessels, and with special stains, both intracellular and extracellular yeast may be seen. Patients often show a rapid clinical improvement within 1—2 weeks, and itraconazole can then replace amphotericin B to complete at least 6—12 months of treatment []. Patients with illnesses that result in profound and prolonged immune suppression should receive long-term suppressive therapy with itraconazole after the initial treatment course is complete.

In patients with recurrent episodes of cellulitis, risk factors should be addressed and consideration given to prophylaxis. Cellulitis is simply defined as an acute infection of the skin involving the dermis and subcutaneous tissues.

Erysipelas classically refers to a more superficial cellulitis of the face or extremities with lymphatic involvement, classically due to streptococcal infection. Diabetic foot infections and wound infections are specific entities. Although they may share some features with cellulitis, their management is different and beyond the scope of this article.

This article will focus on cellulitis of the lower limb. In —5, cellulitis was listed as a primary diagnosis for , completed consultant episodes in secondary care and 75, inpatient admissions with a median length of stay of 3 days with a mean patient age of Many more cases are treated in primary care. Gram-positive cocci such as Streptococcus spp and Staphylococcus aureus are thought to be the predominant cause of cellulitis.

Animal bites can be associated with cellulitis due to Gram-negatives such as Pasteurella and Capnocytophaga. Exposure of a skin break to salt or fresh water is associated with Vibrio vulnificus and Aeromonas spp respectively.

Group A streptococci can be associated with the development of necrotising fasciitis, although this can also be due to mixed infection including Gram-negative and anaerobic organisms, particularly in the elderly and immunosuppressed. The classic presentation of rubor redness , dolor pain , tumor swelling , calor heat are the hallmarks of cellulitis. The spectrum of severity ranges from localised erythema in a systemically well patient to the rapidly spreading erythema and fulminant sepsis seen with necrotising fasciitis.

Pain out of proportion to the clinical signs, in particular, if accompanied by a history of rapid progression should prompt consideration of a necrotising fasciitis. Recent antibiotic exposure and hospital contact should prompt the consideration of antibiotic resistance in the causative organism. Careful clinical examination may reveal a portal of entry such as ulcers, trauma, eczema or cutaneous mycosis.

Skin breaks, lymphedema, venous insufficiency, tinea pedis and obesity have been associated with an increased risk of lower limb cellulitis in case control studies.

Assessment of baseline liver and renal function may be useful for assessing end-organ dysfunction in patients with sepsis and for dosing of antimicrobials. Cultures of blood, aspirates or biopsies are not recommended but should be considered in patients who have systemic features of sepsis, who are immunosuppressed or for cases associated with immersion injuries or animal bites.

While the British Society for Antimicrobial Chemotherapy BSAC expert panel recommendations and UK Clinical Resource Efficiency Support Team CREST guidelines recommend use of the Eron classification of cellulitis in order to grade severity, 15,16 the lack of a clear definition of systemic sepsis and ambiguous and potentially overlapping categories have hampered its use in clinical practice. Marwick et al used a modified version of the Eron classification the Dundee classification to separate patients into distinct groups based on the presence or absence of defined systemic features of sepsis, the presence or absence of significant comorbidities and their Standardised Early Warning Score SEWS.

The SEWS is a standardised form of early warning score, calculated from the patient's routine clinical observations, with a threshold score of 4 selected to indicate the most severely unwell patients class IV in whom a clinical review was mandated at the site where the study was undertaken.

Marwick et al used the Dundee criteria to grade severity and then assessed the appropriateness of the prescribed antimicrobial regimens. These findings suggest the currently used severity scoring system is not a robust means of guiding empirical therapy. There was no significant difference in antimicrobial therapy or treatment outcomes between class I and II severity patients, suggesting that these two groups could be merged, further simplifying the classification. Other severity and prognostic scoring systems for skin and soft tissue infections have been proposed but have yet to be validated.

Suspected sepsis — high-risk criteria a. Available from www. Subject to Notice of rights. All NICE guidance is subject to regular review and may be updated or withdrawn. Patients with purulent skin and soft tissue infections such as abscesses, furuncles or carbuncles should have those collections incised and drained.

Samples should be sent for bacterial culture and consideration given to systemic antibiotics in patients with systemic signs of infection. Non-purulent skin and soft tissue infections generally require treatment with systemic antimicrobials.

Oral antimicrobial therapy is adequate for patients with no systemic signs of infection and no comorbidities Dundee class I , some Dundee class II patients may be suitable for oral antibiotics or may require an initial period of intravenous IV therapy either in hospital or via outpatient antimicrobial therapy OPAT. Intravenous agents should be used for those with evidence of systemic infection Dundee class III and IV or those who do not respond to initial oral therapy.

Patients in whom there is a concern of a deep or necrotising infection should have an urgent surgical consultation for consideration of surgical inspection and debridement. While recommendations regarding specific antimicrobial agents will vary depending on local practice and resistance rates, suggested empiric regimens are outlined in Table 2.

Patients with mild to moderate cellulitis should be treated with an agent active against streptococci. In patients with a history of penetrating trauma or with a purulent infection, the addition of anti-staphylococcal cover is strongly advised. Specific situations, such as infections associated with human or animal bites, may require broader spectrum antimicrobial cover and should be discussed with an infection specialist, as should cellulitis involving atypical sites such as the face, torso and upper limb.

Patients with severe or necrotising infections should have initial broad spectrum antimicrobial cover to include staphylococci, streptococci, Gram-negative organisms and also an agent with activity against toxin production in group A streptococci, such as clindamycin or linezolid. There is little evidence to support the historical practice of adding benzylpenicillin to flucloxacillin in the treatment of cellulitis.

Outpatient parenteral antimicrobial therapy has become an increasingly important means of delivering ambulatory care. The optimal duration of antimicrobial therapy in cellulitis remains unclear. Most cases of uncomplicated cellulitis are traditionally treated with 1—2 weeks of antimicrobial therapy. Patients with three to four episodes of cellulitis per year despite addressing predisposing factors could be considered for prophylactic antimicrobial therapy so long as those factors persist.

National Center for Biotechnology Information , U. Journal List Clin Med Lond v. Clin Med Lond. Tadhg Sullivan , specialist registrar in infectious diseases and microbiology A and Eoghan de Barra , consultant in infectious diseases, senior lecturer B, C.

Author information Copyright and License information Disclaimer. Email: ku. All rights reserved. This article has been cited by other articles in PMC. Key points Making the correct diagnosis is key to management.

Non-infectious conditions should be considered Narrow spectrum penicillins targeting streptococci and staphylococci in the case of purulent infection should be the mainstay of antimicrobial therapy The natural history of cellulitis is one of slow resolution. Management should include limb elevation and continuing narrow-spectrum antimicrobial therapy alongside treatment of comorbid conditions exacerbating the cellulitis oedema, diabetes, vascular disease Outpatient parenteral antimicrobial therapy OPAT including ambulatory care is often appropriate in patients requiring intravenous therapy, but presents challenges in terms of antimicrobial agents used.

Daily review and early switch to oral therapies is optimal In patients with recurrent episodes of cellulitis, risk factors should be addressed and consideration given to prophylaxis. Introduction Definition Cellulitis is simply defined as an acute infection of the skin involving the dermis and subcutaneous tissues. Burden of disease In —5, cellulitis was listed as a primary diagnosis for , completed consultant episodes in secondary care and 75, inpatient admissions with a median length of stay of 3 days with a mean patient age of Microbiology Gram-positive cocci such as Streptococcus spp and Staphylococcus aureus are thought to be the predominant cause of cellulitis.

Clinical presentation The classic presentation of rubor redness , dolor pain , tumor swelling , calor heat are the hallmarks of cellulitis. Box 1. Key points in history taking a. Pattern and speed of progression Age and medical comorbidities diabetes, chronic kidney disease, hepatic disease, vascular disease, immunosuppression Recent antimicrobial treatment Possible site of inoculation — trauma, fungal infections History of previous cellulitis Travel history Risk for atypical organisms: profound immunosuppression animal or human bites sea or freshwater exposure to broken skin including pools and spas exposure to animals, fish, or reptiles intravenous drug use including skin-popping.

Open in a separate window. Risk factors Skin breaks, lymphedema, venous insufficiency, tinea pedis and obesity have been associated with an increased risk of lower limb cellulitis in case control studies.