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Case Report

Serratia marcescens Cellulitis: A Case Report and Review of the Literature

Crum, Nancy F. MD; Wallace, Mark R. MD

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Infectious Diseases in Clinical Practice: December 2002 - Volume 11 - Issue 9 - p 550-554
doi: 10.1097/01.idc.0000090385.89010.75
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Abstract

Serratia was unrecognized as a human pathogen until the 1960s; since then, it has increasingly been noted as a cause of opportunistic infections. Respiratory and urinary tract infections are most common; meningitis, bacteremia, endocarditis, peritonitis, osteomyelitis, and skin infections are occasionally reported. 1 Most infections are nosocomial in origin and are spread through hand-to-hand contact by healthcare providers; cases due to contaminated medical equipment or solutions, including benzalkonium chloride antiseptic, are well described. 1–4Serratia infections are usually associated with an underlying predisposition, such as renal failure, surgery, or instrumentation, steroid use, and prior antibiotic therapy. 5 We describe a case of Serratia marcescens cellulitis in an outpatient and provide a review of the relevant literature.

CASE REPORT

An 81-year-old man with progressive renal failure and multiple medical problems presented with erythema, warmth, and swelling of his right lower extremity. The admission physical examination revealed normal vital signs with cellulitis extending from his right ankle to knee without crepitus, fluctuance, or lymphadenitis. Bilateral hyperpigmentation and leathery skin due to peripheral vascular disease were noted with an arterial brachial index of 0.9. The remainder of examination was unremarkable. He had been admitted twice in the past 2 months for bilateral lower extremity cellulitis and gout. On both occasions, blood cultures were negative, and he was successfully treated with intravenous cefazolin and oral prednisone.

Laboratories demonstrated a white blood count of 26,900/mm3 with 93% neutrophils and 2% band forms, hemoglobin of 10 mg/dL, creatinine of 4.5 mg/dL, bicarbonate of 16 mmol/L, and lactate of 4.6 mmol/L. His urinalysis, urine culture, and chest radiograph were unremarkable. The patient was empirically treated with intravenous cefazolin 1 g twice daily. Blood cultures drawn before antibiotic therapy were positive for S. marcescens (resistant to ampicillin and first-generation and second-generation cephalosporins; sensitive to third-generation and fourth-generation cephalosporins, levofloxacin, meropenem, gentamicin, and trimethroprim-sulfamethoxazole). Blood cultures were repeated, and the patient was switched from cefazolin to cefepime 1 g twice daily and levofloxacin 250 mg daily. Blood cultures taken after 36 hours of cefazolin therapy remained positive for Serratia; after institution of cefepime and levofloxacin, the blood cultures were negative.

A radiograph of the lower extremity and a bone scan were normal. Doppler ultrasound did not reveal any deep venous thrombosis. A transthoracic echocardiogram was negative for vegetations. The cellulitis steadily improved, and the leukocytosis has resolved. However, significant cardiac and pulmonary problems precluded hemodialysis, and he succumbed to progressive renal failure on hospital day 10.

S. marcescens, previously called Chromobacterium prodigiosum, is an opportunistic pathogen of increasing importance. Before Serratia was recognized as a human pathogen in the 1960s, it was used for its distinctive pigmentation as a biologic marker. Interestingly, most human infections are caused by nonpigmented strains. 1 Unlike other Enterobacteriaceae, this organism typically colonizes the respiratory or urinary tracts and most commonly causes infections in these organ systems. Serratia may cause a variety of other infections, including osteomyelitis, septic arthritis (especially after intraarticular injections), endocarditis (particularly in intravenous drug users), and, rarely, cellulitis or necrotizing fasciitis. Soft tissue infections due to gram-negative organisms are relatively uncommon and usually occur in immunocompromised hosts, particularly those with diabetes, malignancy, steroid use, or renal failure.

Serratia infections are most commonly acquired within the hospital, but community-acquired cases may occur, as the organism is ubiquitous and found in soil, sewage, and water. In a study of hospitalized patients with Serratia bacteremia, predisposing features included a recent history of antibiotic use (most often first-generation cephalosporins), surgery, instrumentation, steroid use, or diabetes mellitus. 5 Among community-acquired Serratia soft tissue infections, common risk factors include a history of trauma, renal failure, diabetes, and chronic leg ulceration. 6 Soft tissue infections usually involve areas of broken skin.

We conducted a MEDLINE search for the period 1966-2002, including both English and non-English literature (using the search words Serratia, marcescens, cellulitis, necrotizing fasciitis, necrosis, and soft tissue infections) and identified only 15 cases of community-acquired S. marcescens soft tissue infections (Table 1). 6–16 The number of reported cases increased during the 1990s, although cases were still, overall, uncommon. The median age of the patients was 60 years (range 8-88 years), with 62% of cases occurring in men. Fourteen (88%) cases had a risk factor cited for the development of the Serratia infection; most cases had multiple risk factors. Steroid use was reported in 4 (25%), renal failure in 4 (25%), and diabetes in 3 (19%). The site of the soft tissue infection was most commonly the lower extremity (75%); 3 (19%) cases involved the hand and 1 (6%) case the trunk. Ten (63%) of the Serratia soft tissue infections were cellulitis and 6 (27%) were necrotizing fasciitis.

T1-5
Table 1:
S. marcescens Cellulitis or Necrotizing Fasciitis Cases, 1966 to present

The source of Serratia soft tissue infections was usually from broken skin; skin integrity was compromised by vascular disease and/or ulceration, 5 previous biopsy or surgical site, 3 and trauma. 3 Colonization and infection of the skin may occur during previous hospitalizations and may be enhanced by the use of antimicrobials to which Serratia is resistant. In our case, cellulitis developed in the patient’s lower extremity at the site of ulcerations due to vascular disease. His risk factors included recent hospitalizations, antibiotic therapy with cefazolin, and an immunocompromised state due to progressive renal failure and steroid use. Pulmonary secretions, catheter sites, and the urinary tract may be the source in some cases. In a case report, the sputum harbored Serratia 1 month prior to the development of necrotizing fasciitis of the lower extremity; both organisms had identical antibiograms. 15 The portal of entry in another case was an infected intravenous catheter with bacteremia leading to the development of cellulitis at a distant site. 7 Despite an extensive workup to locate other sources of the Serratia bacteremia in our case, including urinary and sputum cultures, chest radiograph, and echocardiogram, no source other than the soft tissue infection was found, and there were no positive cultures for Serratia during his previous hospitalizations. We postulate that our patient became colonized during 1 of his recent hospitalizations and developed Serratia cellulitis at the site of a leg ulcer due to peripheral vascular disease and subsequently developed bacteremia.

Seven of the 16 (44%) reported that Serratia soft tissue infections developed bullae, a feature most often caused by β-hemolytic streptococci or Staphylococcus aureus. The first description of Serratia bullous cellulitis was in 1983 by Bonner and Meharg 8; in their report, however, it is unclear if Serratia produced the bullae formation, because S. aureus was also isolated from the wound. Subsequent cases have demonstrated that Serratia does cause bullous soft tissue infections. 6,12–15Serratia has been shown to lift off the keratinized layer in a rat model, which may account for its ability to form bullae. 17

Additional clinical features of gram-negative soft tissue infections cited in the literature include limited pain relative to the examination findings and a high likelihood of developing septic shock. 8 One fourth of the reported cases developed septic shock; 2 were associated with cellulitis and 2 with necrotizing fasciitis. Serratia may secrete a proteinase that leads to tissue necrosis and increased vascular permeability, explaining the organism’s ability to cause both necrotizing fasciitis and septic shock. 17

Similar to many Enterobacteriaceae, Serratia has acquired many resistance factors; therefore, the treatment of choice depends on the antibiogram of the isolate. Aminoglycosides were previously the agents of choice; however, due to the development of resistance in the 1970s and the availability of other less toxic agents, these agents are infrequently used. Third-generation and fourth-generation cephalosporins, carbapenems, aztreonam, and fluoroquinolones are now the agents of choice. 18 In this review, almost one half of patients was begun on an initial antibiotic regimen that did not cover Serratia. First-generation and second-generation cephalosporins, clindamycin, and vancomycin, which are frequently used to treat cellulitis, are typically ineffective against Serratia. Surgery is often necessary. Of the 16 cases reviewed, 6 (38%) underwent debridement, 2 (12%) incision and drainage, and 2 (12%) amputation; 6 (38%) patients had no surgical procedures to manage their infection. Four (25%) patients required skin grafting.

The overall mortality rate was 31% in all cases; however, the mortality from the Serratia infection excluding other causes of death was 19%, and all deaths occurred in those with necrotizing fasciitis or septic shock. Of the 6 cases of necrotizing fasciitis, the mortality rate was 50%; this rate may be higher than the mortality rate cited for necrotizing fasciitis by Elliott et al. 19 Underlying medical conditions and an increased age may account for the increased mortality rate in patients with Serratia soft tissue infections.

Gram-negative bacilli, including Serratia, should be considered in cases of cellulitis and necrotizing fasciitis, especially in immunocompromised persons with renal failure, steroid use, or diabetes. Lack of response to narrow-spectrum agents, such as first-generation cephalosporins, bullae formation, or a rapid clinical course, should heighten the suspicion for S. marcescens. Treatment includes broad-spectrum agents such as the third-generation or fourth-generation cephalosporins; prompt surgical intervention may be necessary in some cases.

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© 2002 Lippincott Williams & Wilkins, Inc.