Shewanella algae : A Rare Cause of Necrotizing Fasciitis

Case Report

A 72-year-old male presented to the outpatient wound care center 1 wk after the onset of gradually worsening pain, redness, and swelling of his right lower extremity, together with fever and palpitations. His medical history included hypertension, atrial fibrillation treated with oral anticoagulants, chronic venous stasis, an ulcer of the right leg, and morbid obesity (body mass index [BMI] 38 kg/m²). He reported no history of recent travel, chemical exposure, animal contact, cancer, or intravenous drug abuse. He reported swimming for 1 h at a beach in New York City about a week before his current presentation. Shortly after the swim, he noticed redness of his right leg and a foul-smelling odor emanating from the site of his prior ulcer. His primary care provider prescribed a regimen of dicloxacillin 500 mg PO q6h, but this failed to produce any improvement after 4 d of therapy.

On examination, the patient's vital signs were as follows: temperature 101°F, heart rate 115 beats/min (irregularly irregular), blood pressure 120/50 mm Hg, respiratory rate 22 breaths/min, and O₂ saturation 95% on room air. Inspection of the patient's right leg revealed a 1-cm by 1-cm tender, weeping ulcer on the anterolateral aspect of the mid-leg. with surrounding blanching erythema and calor involving the mid- to distal third of the leg. A gray, foul-smelling discharge could be expressed manually from the ulcer. There was extensive lipodermatosclerosis and 3+ pitting edema without crepitus. Aside from the 3+ pitting edema and mild lipodermatosclerosis, the patient's left lower extremity was unremarkable. He had palpable pedal pulses bilaterally.

The patient was admitted urgently to the emergency department, where prompt intravenous fluid resuscitation was initiated. Blood and urine cultures were obtained with plans to obtain definitive cultures from the patient's wound in the operating room. Laboratory studies were notable for a white blood cell (WBC) count of 22,600/mcL with 90% polymorphonuclear leukocytes (PMN); a serum sodium concentration of 136 mEq/L; lactic acid concentration of 2 mmol/L; and bicarbonate concentration of 20 mEq/L with a base deficit of 0.5 and an anion gap of 13. No other laboratory abnormalities were noted. Treatment of the patient with broad-spectrum antibiotics was begun with vancomycin and piperacillin-tazobactam. He remained stable hemodynamically, during the initial resuscitation period and was taken directly to the operating room for surgical debridement.

Intraoperatively, extensive necrosis and gangrene were noted throughout the subcutaneous tissues underlying the patient's ulcer, together with disruption of the adjacent fascial planes. Myonecrosis of the underlying muscular beds was noted. All non-viable tissue and suppurative foci were debrided widely and sent for gram staining and culture. Permanent samples were also sent in formalin solution for histologic evaluation. Debridement was performed until viable bleeding tissue was encountered. Surgical hemostasis was obtained. The surgical wound was then packed thoroughly with sterile gauze soaked in a 0.5% sodium hypochlorite/0.4% boric acid suspension (Dakin Solution, Century Pharmaceuticals, Indianapolis, IN) and covered with petrolatum- and bismuth tribromophenate-impregnated gauze (Xeroform, Covidien, Mansfield, MA). The patient tolerated the procedure well without any complications, and was transferred to the surgical intensive care unit (SICU) for further care.

Within 36 h a gram-negative bacillus was isolated from the patient's initial peripheral blood cultures, and within 72 h S.algae was confirmed by Kirby-Bauer disk diffusion. The microorganism was shown to be susceptible to piperacillin-tazobactam. The patient's treatment with vancomycin was discontinued.

On post-operative day one, inspection of the patient's wound revealed a viable, bleeding, granulating base with moderate fibrinous exudate and superficial fat necrosis without frank purulence. No further debridement or cultures were deemed necessary at this time. After 72 h of meticulous wound care and dressing changes with Dakin solution-soaked gauze, we noted a decreased amount of exudative debris. On post-operative day four the decision was made to proceed with use of a vacuum-assisted closure device (VAC), using silver-impregnated applicators. These were changed every 72 h. Wound healing progressed favorably over the course of the next 10 d, with the development of healthy granulation tissue at the base of the wound. The final report on the permanent pathology specimen obtained noted severe acute inflammation and necrosis of the skin, subcutaneous tissue, and underlying fascia.

The patient was discharged to a subacute rehabilitation facility for continued wound care, intravenous antibiotic therapy, and physical rehabilitation [10]. He was seen on a weekly basis in the office for dressing changes. Given the absence of fever and the patient's continued clinical improvement, antibiotics were discontinued at the time of the first post-operative outpatient visit, 14 d after his surgery. With a viable, well-granulating wound base, he underwent split-thickness skin graft surgery 1.5 mos after his original surgical debridement and had no complications (including donor site complications) from this, and his original wound proceeded to complete healing.

Discussion

Necrotizing soft tissue infection is characterized by rapidly progressive necrosis involving the subcutaneous tissues. Necrotizing fasciitis specifically describes extension of the infection along deep fascial planes, lymphatic channels, and the venous system, causing microvascular thrombosis, focal venous congestion, and tissue necrosis [11]. High-virulence, exotoxin-producing organisms such as Group A streptococci (Streptococcus pyogenes) or Clostridium perfringens are typical causes of NF. Given our comprehensive review of the literature in relation to the case reported here, this case may reflect the geographic spread and emergence of S. algae infection in the United States. Clinicians must be aware of the potential for NSTIs even in immunocompetent hosts. One plausible virulence factor for this spread is the organism's production of bacterial hemolysin, which may have direct cytotoxic effects on the basis of findings during its prolonged incubation on sheep blood agar [9]. By contrast to that of S. putrefaciens, the ability of S. algae to grow at 42°C in 6% NaCl and to reduce nitrite make it a highly adaptable organism capable of surviving in a variety of different micro-environments [12]. Others suggest that the organism produces an exotoxin that, in a manner similar to that of P. aeruginosa, serves to destroy macrophages prior to phagocytosis. This may explain the proclivity of S. algae for causing the severe disease that it does cause even in the immunocompetent host [13,17].

Historically, S. algae has been susceptible in vitro to carbapenems, erythromycin, aminoglycosides, and fluoroquinolones, but has shown significant resistance to penicillins [2,14]. A chromosome-encoded beta-lactamase may be responsible for the relative resistance to penicillin antibiotics in both S. algae and S. purefaciens [15]. However, one of the most important differences between S. algae and S. putrefaciens is the former's apparent resistance to colisitin [12].

Although S. algae has been reported to cause soft tissue infections in immunocompromised patients and under unsanitary or crowded conditions, we did not find any reports in the English-language literature of NF in an immunocompetent individual in the United States. A major risk factor for the development of NF in our patient was chronic venous stasis. Elevated venous pressures and stretching of the veins in the lower extremities results in the transudation of inflammatory mediators into the subcutaneous tissues. These mediators destroy subcutaneous tissue and overlying skin via deficiencies in fibrinolysis, leading to microvascular thrombosis, end-organ ischemia, and the release of reactive oxygen species [16]. Furthermore, defective venous drainage may promote ischemic damage by two mechanisms: (1) Accumulation of leukocytes in blood vessels, and (2) leakage of fibrinogen from veins, causing fibrin accumulation around vessels and preventing growth factors, molecules in the extracellular matrix, and oxygen from reaching distal tissues. Also, local edema serves as a nidus for rapid proliferation after bacterial colonization, leading to infection and subsequent tissue necrosis.

Conclusion

Shewanella algae is an organism with substantial pathogenic potential that has been reported to cause life-threatening bacteremia, cellulitis, and acute exacerbations of chronic otitis media, and in the present case was causative of NF, even in immunocompetent hosts. Clinicians should be aware of this highly virulent organism with the potential for life-threatening NSTI in patients with known risk factors and suggestive exposures.