Dermatology Online Journal

Serratia marcescens folliculitis and concomitant acne vulgaris
Stephanie Lehrhoff MD, John Yost MD, Maria Robinson MD, Rishi Patel MD, Miguel Sanchez MD
Dermatology Online Journal 18 (12): 19

The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York, New York

---

Abstract

We present a unique case of S. marcescens folliculitis of the trunk in a 46-year-old woman with a history of facial acne vulgaris during her teen years. Her eruption occurred at the time of elective ambulatory surgery when she was treated with pre and post-operative antibiotics. The diagnosis of S. marcescens folliculitis was made on the basis of histopathologic features and tissue culture of a skin biopsy specimen of a pustule after her eruption was unresponsive to conventional treatment for inflammatory acne vulgaris. The history and pathophysiology of gram-negative folliculitis in the setting of acne vulgaris is reviewed.

---

History

A 46-year-old Moroccan woman presented to the Dermatology Clinic at Bellevue Hospital Center in September, 2011, with a three-month history of erythematous papules and pustules with many open and closed comedones that were scattered on back and chest. The eruption began around the time of breast reduction surgery. At the time of her breast reduction surgery, she was given one gram of intravenous cefazolin preoperatively and discharged on one week of oral cephalexin 500 milligrams every six hours. She reported acne of her face during her teenage years. However, she had not had acne of her face, chest, or back since that time. During her initial visit to the dermatology clinic, oral doxycycline 100 mg, topical clindamycin phosphate solution, and benzoyl peroxide 10 percent wash twice daily were started. Two months later, she returned for further evaluation. She reported no improvement with the prescribed therapy and believed the eruption was worsening. A punch biopsy was performed.

Our patient was treated with a two-week course of oral ciprofloxacin, which led to resolution of the pustules. However, rare, erythematous, inflammatory papules continue to occur over the entire back and many open and closed comedones remain. She is currently being treated with topical tazarotene 0.1 percent gel nightly, benzoyl peroxide 10 percent wash, and a single 20 percent salicylic acid peel of the back with a modest response. A trial of oral isotretinoin is under consideration if the current therapies prove inadequate.

Physical examination

Figure 1	Figure 2

Many erythematous papules and a few pustules extended from the nape of the neck to the pre-sacrum and included both the medial and lateral aspects of the back. Many open and closed comedones were found on the upper back. There were also sparsely scattered, erythematous papules and closed comedones on the upper chest and shoulders. The face was spared of active involvement, but showed a few ice-pick scars on the cheeks.

Laboratory data

Tissue culture of a punch biopsy specimen of a pustule from the right mid back grew Serratia marcescens. The strain of S. marcescens was resistant to cefazolin and cefuroxime. The strain of S. marcescens had intermediate sensitivity to tetracycline and cefoxitin.

Histopathology

Figure 3

Within the dermis there is a perivascular and interstitial infiltrate of neutrophils with scattered eosinophils. There is a slightly dilated follicular ostium with small numbers of yeast forms. A period acid-Schiff and diastase stain fails to reveal fungal hyphae and a Gram stain fails to reveal bacteria.

Discussion

Gram-negative folliculitis in acne vulgaris was first described in 1968 in a series of patients with gram-negative superinfection of facial pustules in the setting of treatment refractory acne vulgaris. These patients developed papules and pustules that were concentrated around the nares after long-term use of antibacterial soap and various systemic antibiotics [1]. Male predominance, oily skin type, a perioral or perinasal distribution, and prolonged antibacterial treatment are common features of acne patients with gram-negative folliculitis [1]. There are two types of gram-negative folliculitis in acne vulgaris. Type I is characterized by small, three-to-six-millimeter, erythematous papules and pustules spreading out from the anterior nares. Larger and deep-seated, fluctuant, cystic nodules that are caused by Proteus mirabilis are characteristic of type II gram-negative folliculitis [2]. In a series of 46 patients with gram-negative folliculitis, the most frequently cultured organisms included Klebsiella spp., Escherichia coli, Enterobacter spp., and Proteus spp [3].

Replacement of the resident gram-positive bacterial flora within the nares and facial skin by pathogenic gram-negative organisms is thought to underlie this disease [4]. Gram-negative bacterial growth depends on a moist environment. Overproduction of sweat and sebum creates a favorable environment for the growth of gram negative rods. Isotretinoin, which is the first line treatment for this condition, is effective by causing a decrease in sebum production [5, 6]. Various immune mechanisms also may play a role in the pathogenesis. A depressed cell-mediated immunity with weak or absent delayed-type hypersensitivity responses was found in a minority of patients with gram-negative folliculitis. A weak humoral immunity, which may occur in patients with selective IgM deficiency who are prone to septicemia from gram-negative bacteria, also has been hypothesized to contribute to susceptibility to these infections. Fittingly, depressed levels of IgM have been found in a cohort of patients with gram-negative folliculitis. Depressed alpha-1 antitrypsin levels, which are implicated in impaired C3 activity, important in opsonization and lysis of bacteria, was found in more than one-half of gram-negative folliculitis patients [3]. In addition to weakened host defense immunity, tetracycline antibiotics have been implicated in impairing protein synthesis and functioning of human lymphocytes as well as inhibiting chemotaxis of neutrophils. These effects enhance the risk of bacterial superinfection [7, 8].

Gram-negative folliculitis may also develop de novo, without concomitant acne and without preceding antibacterial treatment [4]. There are a few reports of skin and soft tissue infection that are attributed to Serratia marcescens, which is a colonizer of the respiratory and genitourinary tracts. S. marcescens has been implicated in cases of cellulitis, abscesses, necrotizing fasciitis, secondary infection of leg ulcers, and dissemintated papular erosions among others [9-14].

We present a unique case, which to our knowledge has previously not been described, of S. marcescens folliculitis of the trunk in a 46-year-old woman with history of facial acne vulgaris. This infection occured after ambulatory elective surgery and administration of prophylactic intravenous antibiotics and oral cephalexin. The diagnosis of S. marcescens folliculitis was made on the basis of the culture and histopathologic features of a skin biopsy specimen from a pustule after her eruption was unresponsive to conventional treatment for inflammatory acne vulgaris. The tissue culture grew S. marcescens that was resistant to several first and second generation cephalosporins. The bacteria showed intermediate sensitivity to tetracycline and cefoxitin. This finding suggests that our patient developed gram-negative folliculitis as a result of the replacement of her commensal skin flora with the gram-negative Serratia marcescens after the administration of pre and post operative first generation cephalosporin antibiotics. In addition, her lack of response to oral doxycycline is expected, owing to the intermediate sensitivity of her S. marcescens strain to tetracycline.

References

1. Fulton JE, et al. Gram-negative folliculitis in acne vulgaris. Arch Dermatol 1968; 98: 349 [PubMed]

2. Leyden JJ, et al. Gram-negative folliculitis: a complication of antibiotic therapy in acne vulgaris. Br J Dermatol 1973; 88:533 [PubMed]

3. Neubert U, et al. Bacteriologic and immunologic aspects of gram-negative folliculitis: a study of 46 patients. Int J Dermatol 1999; 38: 270 [PubMed]

4. Böni R, et al. Treatment of gram-negative folliculitis in patients with acne. Am J Clin Dermatol 2003; 4: 273 [PubMed]

5. Landthaler M, et al. Inhibitory effects of 12-cis retinoid acid on human sebaceous glands. Arch Dermatol Res 1980; 269:297 [PubMed]

6. James WD, et al. Treatment of Gram-negative folliculitis with isotretinoin: positive clinical and microbiologic response. J Am Acad Dermatol 1985; 12: 319 [PubMed]

7. Forsgren A, et al. Influence of antibiotics on lymphocyte function in vitro. Infection 1978;6:91.

8. Esterly NB, et al. Neutrophil chemotaxis in patients with acne receiving oral tetracycline therapy. Arch Dermatol 1984; 120: 1308 [PubMed]

9. Bogaert MA, et al. Serratia celluitis and secondary infection of leg ulcers by Serratia. J Am Acad Dermatol 1991; 25:565. [PubMed]

10. Nieves DS, et al. Painful red nodules of the legs: a manifestation of chronic infection with gram-negative organisms. J Am Acad Dermatol 1999; 41: 319 [PubMed]

11. Friedman ND, et al. Spontaneous dermal abscesses and ulcers as a result of Serratia marcescens. J Am Acad Dermatol 2003; 49: S193 [PubMed]

12. Munoz-Perez MA, et al. Disseminated popular eruption caused by Serratia marcescens: a new cutaneous manifestation in HIV-positive patients. AIDS 1996; 10: 1179 [PubMed]

13. Bachmeyer C, et al. Necrotizing fasciitis due to Serratia marcescens. Clin Exp Dermatol 2004; 29: 673 [PubMed]

14. Joăo AM, et al. Recurrent Serratia marcescens cutaneous infection manifesting as painful nodules and ulcers. J Am Acad Dermatol 2008; 58: S55 [PubMed]

© 2012 Dermatology Online Journal