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Facial cellulitis associated with complicating ophthalmic herpes zoster

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Facial cellulitis associated with Pseudomonas aeruginosa complicating ophthalmic herpes zoster
Laura Atzori MD1, Caterina Ferreli MD1, Myriam Zucca MD1, Daniela Fanni MD2, and Nicola Aste MD1
Dermatology Online Journal 10 (2): 20

1. Clinica Dermatologica - Università di Cagliari. lauratzori@tin.it
2. I Cattedra di Anatomia Patologica – Università di Cagliari via Ospedale 54 - 09124 Cagliari (Italy)


Abstract

Cellulitis is a rare and severe soft-tissue infection characterized by acute, diffuse, spreading inflammation, often associated with systemic symptoms such as malaise and fever. Surgery of the head and neck, dental infections, sinusitis, upper respiratory tract infections, and trauma are the most common portal of entry for pathogens in facial cellulitis. A very unusual case complicating an ophthalmic herpes zoster in a 74-year-old woman was observed at the department of dermatology, Cagliari University (Italy). Culture of skin swabs showed growth of numerous Gram-negative bacilli, further identified as Pseudomonas aeruginosa. Therapy with intravenous ciprofloxacin was promptly instituted on the basis of the culture and sensitivity report. She was initially treated with daily drainage and twice-daily topical fusidic acid. The lesion completely resolved in 4 weeks, and no general complications or recurrence have been observed for 6 months. Early recognition and management of facial cellulitis is mandatory to avoid serious and generalized complications. Pseudomonas aeruginosa is rarely reported in facial cellulitis; there are apparently no reports of this infection occurring as a complication of ophthalmic herpes zoster. Herpetic damage of the anatomic barrier as well as impairment of defense mechanisms because of decompensated diabetes mellitus may have facilitated the colonization and proliferation of this opportunistic pathogen in our patient.



Introduction

Varicella zoster is a common infection worldwide with a generally benign course, especially because the availability of specific antiviral treatment. Cellulitis is a severe, acute soft-tissue infection characterized by rapidly spreading erythema that progresses to abscess formation and is usually accompanied by malaise and fever [1, 2, 3]. Precipitating factors are usually necessary to allow pathogen invasion of the dermis and subcutis; in the facial region the most common portals of entry are dental infections, sinusitis, upper respiratory tract infection, surgery, and trauma [3, 4, 5]. Other conditions predisposing to cellulitis are malignancies, chemotherapy (especially when associated with persistent leukopenia), and acquired immunosuppression (AIDS). Cellulitis rarely presents as a cutaneous complication of an oral herpes simplex infection [3]. When it occurs, the responsible organisms are most often Staphylococcus aureus, β-hemolytic Streptococcus, and anaerobic bacteria such as Hemophilus influenzae [4, 5, 6]. Pseudomonas aeruginosa has rarely been reported as responsible for facial cellulitis [4, 5, 6, 7], and never as a complication of ophthalmic herpes zoster. This Gram-negative bacillus is cosmopolitan in distribution of low virulence potential in healthy patients [8, 9]. Local anatomic changes or general impairment of defense mechanisms usually facilitate colonization and proliferation of this opportunistic pathogen. Once the microorganism has passed the mucocutaneous barrier, the risk of life-threatening complications is very high [3].

Early recognition and management of facial cellulitis is mandatory to avoid serious and generalized complications. Antibiotic treatment has to be guided by the culture and sensitivity report (antibiogram), and prompt surgical debridement is also generally required [1, 2, 3, 6, 7, 8, 9].


Clinical synopsis


Figure 1 Figure 2
Erythematous-edematous voluminous tumor involving the left supraorbital and homolateral frontal region, whose surface is interrupted by deep, confluent, undermined ulceration. A dense, yellow, purulent and necrotic material is visible in the fundus of the ulcers (Fig. 1).
Acute inflammatory process, extending throughout the dermis and occasionally into the subcutaneous tissue, characterized by a diffuse mixed infiltrate, composed chiefly of neutrophils, marked edema, dilatation of blood vessels, and focal necrobiosis of fascial collagen fibers. (H&E; 25x) (Fig. 2).

A 74-year-old woman presented to the dermatology department of the University of Cagliari (Italy) with a tender large tumor on her left supraorbital and frontal region. On examination the entire left-supraorbital region appeared occupied by a 6-cm round, erythematosus, edematous tumescence; the surface was interrupted by deep, confluent, undermined ulcerations. The necrotic fundus of these ulcers was filled with dense, yellow, purulent and bloody material (Fig. 1). The lesion was painful and extremely tender to palpation. There was no hyperpyrexia. There was no ocular or mucous membrane involvement; there were no palpable lymph nodes. The patient had been evaluated in the same department about 12 days previously for a typical ophthalmic herpes zoster; she was treated with oral famcyclovir (750 mg daily) with substantial initial improvement. Unexpectedly, the patient noted breakdown and painful swelling of some of the crusted herpetic lesions; these became confluent within few days, forming a subcutaneous abscess. The familial and pathologic history was unremarkable, except for longstanding insulin-dependent diabetes. Preliminary laboratory investigations revealed 11.3 x 109 /L WBC (normal value [nv] 4.00-10.00), erythrocyte sedimentation rate of 88 mm 1st hour; C-reactive protein of 61.1 mg/L (nv < 5); α-2 protein of 21.6 percent (nv 8.5 -15.1 %); fibrinogen 568 mg/dl (nv 150-450). The biochemistry profile was within normal range except for hyperglycemia (basal value 253 mg/dl) despite insulin treatment. Culture of skin swabs grew numerous Gram-negative bacilli, further identified as Pseudomonas aeruginosa sensitive to ciprofloxacin. Repeat blood cultures were negative. Investigation of humoral and cell-mediated immunity showed no major defects. ECG and X-ray of the chest were normal. Examinations of the head and orbit with ultrasound imaging and computerized tomography confirmed the presence of a large inflammatory tumescence involving the soft tissues of the left periorbital region, with a non-homogenous content and gas inclusions. The absence of osteolysis excluded the involvement of the underlying bone. A deep biopsy was performed; histological examination showed an acute inflammatory process with a diffuse mixed infiltrate loosely arranged around dilated blood vessels, and extension throughout the dermis (Fig. 2). Focal necrobiosis was also present, with collagen fibers of the fascia parted and disarranged by edema and infiltrating neutrophils.


Figure 3
Clinical results after treatment.

Intravenous ciprofloxacin (400 mg per day) was started with a rapid improvement; it was continued for 10 days and then changed to oral administration (500 mg twice daily for another 10 days). The antibiogram performed at day 12 showed no bacterial growth. Initial daily drainage was done to remove necrotic, purulent material from the lesion. Topical fusidic acid was applied twice daily until complete second-intent closure occurred for the central ulcer; Healing progressed very slowly and was complete in a 4 weeks, resulting in a slightly fibrous, hypertrophic scar (Fig. 3). No relapse or complications were observed in a 6-month follow-up visit.


Discussion

This case represents a peculiar and severe condition requiring prompt systemic treatment and daily surgical drainage in order to avoid life-threatening complications. Facial cellulitis is a rare infection; it is characterized by an acute inflammatory process involving the dermis and subcutaneous tissue and evolution to abscess formation [1, 2, 3]. Most primary cases are caused by Gram-positive organisms, but secondary forms associated with local infection, trauma, or surgery (especially of the head and neck region) [3, 4, 5, 6] are often polymicrobial, and some cases caused by Pseudomonas aeruginosa have been reported [4, 5, 6, 7]. This ubiquitous Gram-negative bacillus produces infections in many different organs, including the skin and soft tissues; these infections range from minor lesions to potentially life-threatening septicemia. Pseudomonas is rarely able to initiate the pathologic process unless there is a local or general impairment of defense mechanisms [7, 8, 9]. With regard to our patient, herpes zoster lesions provided the disruption of the cutaneous barrier, in spite of early aggressive antiviral treatment. Manipulation, poor hygiene, and the coexistence of uncontrolled diabetes mellitus in this elderly woman might have favored this uncommon infection. No major defect of cellular immunity was detected in our patient, but a minimal dysfunction is putatively responsible for susceptibility to cutaneous infection in diabetic patients[10]. Identification of Pseudomonas aeruginosa as causative agent, with the potentiality to cause septicemia and mortality [3, 6, 7, 8, 9], prompted us to start a systemic treatment. A good therapeutic response ensued, which we attribute to ciprofloxacin, daily drainage to remove purulent and necrotic material from the lesion, and the use of a topical antiseptic agent. The patient recovered, and the only residual was a modest hypertrophic scar that was judged acceptable; no further surgical correction was required.

Facial cellulitis very rarely presents as a complication of herpes zoster. This is the first report in which Pseudomonas aeruginosa is the associated pathogen. Early recognition, appropriate antibiotic treatment, and constant monitoring of the patient are crucial to avoid serious complications.

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