Sir,

Necrotizing fasciitis has received much interest in the media in recent years, due to its rapid progression, gruesome characteristics, and high mortality rate, estimated at 28% in a recent retrospective study.1 Haemolytic streptococci, Staphylococcus aureus, Escherichia coli, pseudomonas, Enterobacter, Klebsiella, Proteus, Bacteroides, Clostridium, and peptostreptococcus are among those species isolated from wound cultures and identified as causative, with streptococcus being the commonest at 62%.1 While necrotizing fasciitis classically involves the trunk, groin, and lower limbs, primary involvement of the eyelids is a well-known entity.2, 3 We describe the first report of Moraxella species being the causative organism in a case of necrotizing fasciitis.

Case report

A 50-year-old male presented with a 4-day history of left periorbital swelling, treated with oral flucloxacillin by his general practitioner. On examination, the left eye was swollen closed, erythematous, exquisitely tender, and hot to touch, but without a drainable or pointing abscess. Cervical lymphadenopathy, a pyrexia of 38.2°C, and tachycardia were noted. Blood tests revealed a raised C-reactive protein of 417, an ESR of 61, and a neutrophilia of 15.8 × 109/l. CT scan did not demonstrate any orbital involvement and excluded sinus disease as a cause. Preseptal cellulitis was diagnosed and intravenous benzylpenicillin and flucloxacillin were commenced; after 2 days without clinical improvement, oral metronidazole was added to the regime. At 4 days after his admission, after initial wound swabs were negative for microscopy and culture, the left eyelid began to develop areas of necrosis (Figure 1). At the same time, the eye was prised open enough to obtain a visual acuity of 6/9 and to establish that the conjunctiva was white and the cornea clear, thus reducing the likelihood of posterior spread of the infection. Surgical debridement took place immediately, down to healthy, bleeding tissue. Histology confirmed the diagnosis of necrotizing fasciitis, with the presence of inflammatory debris, necrotic tissue, and purulent exudates consistent with acute inflammation and necrosis. Culture of the debrided tissue grew Moraxella catarrhalis, and the antibiotic regime was altered to intravenous co-amoxyclav alone on discussion with the microbiologist. On day 11, 1 week after debridement, the patient was discharged home on oral co-amoxyclav, with a healthy, granulating wound. At 3 weeks post-operation, he has the upper lid hung up in down gaze, but no lagophthalmos on gentle eyelid closure, and no corneal staining (Figure 2).

Figure 1
figure 1

Preoperative preseptal cellulitis with tissue necrosis.

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Figure 2
figure 2

3 weeks postoperatively, showing the upper lid hung up in down gaze.

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Comment

Moraxella species, a gram-negative, aerobic, oxidase-positive diplococcus, is a known commensal in the nasopharynx, and a common causative organism of otitis media, sinusitis, and laryngitis. While it has been linked in two cases to pre-septal cellulites,4, 5 no cases of necrotizing fasciitis as a result of infection by Moraxella have been reported in the literature. This may indicate an increase in the pathogenicity of the organism or, as is not uncommon in head and neck fasciitis, the presence of more than one infective agent, the other agent having been successfully treated with flucloxacillin and benzylpenicillin. Diagnosis of necrotizing fasciitis is based on the clinical presentation of pain, erythema, skin necrosis, and oedema, with subsequent histological findings of extensive fascial and subcutaneous tissue necrosis,1 which the above case clearly demonstrated. Due to the increasing prevalence of B-lactamase producing Moraxella strains, explaining the poor response to initial antibiotic treatment, the recommended antibiotic regime is now co-amoxyclav or a cephalosporin (first, second or third generation) on recognition of, or when there is a suspicion of, Moraxella infection.

Emphasis on early surgical debridement of tissue at the first sign of necrosis, and regular dialogue with infectious diseases clinicians and microbiologists, particularly in those patients not responding to intravenous antibiotics, should ensure optimal management of this rare, but potentially life-threatening, condition.