Bacteria-induced nasal necrosis with negative cultures

Background

Pseudomonas putida is a Gram-negative bacillus found commonly in the environment. Its pathological capacity is considered minimal in normal, healthy individuals1; however, it has been found to be a pathological organism in patients with immune compromise or indwelling devices.2 3 We present a case of necrotising P. putida infection of the nasal columella and septum in a patient with fulminant liver failure. A current literature search did not yield any other cases of P. putida specifically in a nasal infection. Reports of P. putida as a pathological infection consist mostly of urinary tract infections2 or bloodstream infections secondary to central venous catheter use3 4; however, some reports do describe its implication in the skin or soft tissue infections as well as meningitis in patients with cancer, neonates or those with mucocutaneous defects.1–3 5–7

Case presentation

A 79-year-old man with liver failure, hypertension and hyperlipidemia presented with a 1.5-month history of progressive nasal crusting. The crusting began 2 weeks after hospitalisation for bronchitis during which he received breathing treatments. Symptoms began with pain and sores on the inside of the nose, which was unresponsive to saline spray and neomycin, progressing to involve the columella and philtrum. He denied epistaxis although the lesions would bleed when aggravated. He denied intranasal drug use. No history of diabetes or use of immunosuppressive therapy. Prior to the presentation culture done by an outside otolaryngologist was negative. On physical examination, dark, dry, crusted debris was visualised on the columella and skin of entrance of the nasal vestibule with healthy granulation tissue below bilaterally (figure 1).

Investigations

On rigid endoscopy, debris extended to middle and inferior turbinate to midway posteriorly. Middle turbinates and mucosa were sensate. No lesions were present on the mouth or palate. A maxillofacial CT scan revealed a possible mucocele on the left middle turbinate but otherwise no abnormality. The patient underwent endoscopic biopsy of the lesion under general anaesthesia for definitive diagnosis; intraoperative findings included gross nasal crusting and inflammation involving the nares bilaterally, the nasal columella and extending intranasally to the anterior, middle and inferior turbinate on the right.

Histopathological findings revealed abundant acute inflammation with minute fragments of atypical squamous epithelium, favouring reactive atypia. Non-invasive fungal hyphae were identified. Bacterial cultures revealed Staphylococcus epidermidis, Corynebacterium accolens, Curvularia species and P. putida.

Differential diagnosis

This patient initially presented with progressive nasal crusting and necrotic-appearing tissues around the nares and columella. Differential diagnoses considered included trauma-induced necrosis from nasal cannula oxygen use as well as sinonasal lymphoma and invasive fungal sinusitis. CT scan did not reveal erosion or mass; in addition, symptoms noted to be commonly present in sinonasal lymphoma cases such as rhinorrhea, epistaxis and obstruction and physical examination findings such as ulcerated or polypoid intranasal mass were absent. Our patient displayed only necrosis.8 Fungal invasion remained a consideration until tissue biopsy resulted. This case highlights the importance of reconsidering bacterial infection and obtaining a tissue biopsy in the case of non-healing necrotic-appearing tissue with negative culture swab and CT without evidence of mass.9 While nasal necrosis in neonates secondary solely to trauma from nasal oxygen has been reported, the incidence in adults is far less likely10 11 and secondary causes should be examined.

Treatment

Treatment was undertaken with a 6-week course of intravenous pipercillin–tazobactam as well as topical mupirocin, completed in the outpatient setting with the use of home healthcare and a peripherally inserted central catheter (PICC) line. Although susceptible to PO ciprofloxacin, the patient’s liver team expressed concern for levaquin-associated vanishing bile duct syndrome in the setting of his liver failure.

Outcome and follow-up

With the initiation of the above treatment, the patient improved after a 6-week course (figure 2). Follow-up cultures 2 months after initial culture were negative and PICC was removed.