Zosteriform impetigo: Wolf’s isotopic response in a cutaneous immunocompromised district

Philip R. Cohen1

1 Department of Dermatology, University of California San Diego, CA, USA

Key words: cutaneous, dermatome, dermatomal, district, herpes, immunocompromised, impetigo, infection, isotopic, response, skin, staphylococcal, Staphylococcus aureus, Wolf, zoster, zosteriform

Citation: Cohen PR. Zosteriform impetigo: Wolf’s isotopic response in a cutaneous immunocompromised district. Dermatol Pract Concept 2015;5(3):9. doi: 10.5826/dpc.0503a09

Received: April 26, 2015; Accepted: May 5, 2015; Published: July 31, 2015

Copyright: ©2015 Cohen. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: None.

Competing interests: The authors have no conflicts of interest to disclose.

All authors have contributed significantly to this publication.

Corresponding author: Philip R. Cohen, MD. Email: mitehead@gmail.com

Abstract

Background: Impetigo can result from Staphylococcus aureus (S. aureus). Wolf’s isotopic response is the occurrence of a new cutaneous disorder at the site of a previously healed disease. A cutaneous immunocompromised district is an area of skin that is more vulnerable than the rest of the individual’s body.

Purpose: To describe a man with impetigo localized to a unilateral dermatome and review the clinical features of other patients with zosteriform Staphylococcus aureus cutaneous infection.

Methods: PubMed was used to search the following terms, separately and in combination: cutaneous, dermatome, dermatomal, district, herpes, immunocompromised, impetigo, infection, isotopic, response, skin, staphylococcal, Staphylococcus aureus, Wolf, zoster, zosteriform. All papers were reviewed and relevant manuscripts, along with their reference citations, were evaluated.

Results: Crusted, eroded and intact, erythematous papules and nodules acutely presented localized to the mandibular branch of the left trigeminal nerve on the face of a 66-year-old man; he did not recall a prior episode of varicella-zoster virus infection in that area. A bacterial culture isolated methicillin-susceptible S. aureus. Viral cultures and direct fluorescent absorption studies were negative for herpes simplex and herpes zoster virus. All of the lesions resolved after oral treatment with cefdinir. Impetigo and/or furunculosis in a zosteriform distribution have also been described in 3 additional patients. The bacterial culture showed either methicillin-susceptible or methicillin-resistant S. aureus; the skin infection resolved after treatment with oral antibiotics; however one man experienced 2 recurrences in the same area.

Conclusions: Zosteriform cutaneous staphylococcal impetigo may be an example of Wolf’s isotopic response in a cutaneous immunocompromised district.

Introduction

Impetigo is a bacterial infection that can be caused by Staphylococcus aureus (S. aureus) [1]. Herpes zoster is a viral infection caused by varicella-zoster virus [2]. Occasionally, non-viral conditions—including bacterial infections—can morphologically mimic herpes zoster by presenting with skin lesions in a dermatomal distribution [3]. A man who presented with zosteriform facial skin lesions of impetigo is described and the clinical features of previously reported patients with dermatomal S. aureus infection are summarized.

Case report

A 66-year-old healthy afebrile man presented for evaluation of skin lesions that had developed on the left side of his face. His cutaneous past medical history was remarkable for cryotherapy-treated actinic keratoses, excision of two basal cell carcinomas (on the left chest in 2004 and the right cheek in 2009), and genital herpes simplex virus type 2 infection. He had chicken pox as a child and no episode of herpes zoster; he had received the varicella vaccine 2 years ago.

A week earlier, he noticed that facial skin lesions began to appear. Initially the site was pruritic and then a crust would develop; there were no blisters. The lesions were first noted on the left side of his chin; subsequently, they developed on his left cheek and left neck, near his jaw. Based on the distribution and morphology of his skin lesions, his wife diagnosed him to have a shingles.

Cutaneous examination showed crusted, eroded and intact, erythematous papules and nodules—ranging in size from 3 to 5 mm in diameter—restricted to only the left side of his face. There were about 12 lesions. They were located on his chin, cheek, and neck in a distribution that corresponded to the third division of the fifth cranial nerve (Figure 1).

Figure 1 (A, B, and C). Distant (A) and closer (B and C) views of zosteriform impetigo located on facial skin innervated by the mandibular branch of the left trigeminal nerve; the lesion appear as crusted, eroded and intact, erythematous papules and nodules on the left side of the chin (B) and neck (C). [Copyright: ©2015 Cohen.]

The unilateral and dermatome location of the skin lesions raised the possibility of herpes zoster. However, the appearance of the individual crusted erosions was consistent with impetigo. Additional laboratory studies were performed and he was empirically treated for both herpes zoster (with 1 gram of oral valacyclovir three times daily for 10 days) and impetigo (with 300 mg of oral cefdinir twice daily for 10 days and topical mupirocin 2% ointment three times daily for 10 days).

All of the facial skin lesions resolved within 1 week; no residual crusts were present at his 1-month follow up examination. A Tzanck smear taken from one of the lesions at presentation was negative for multinucleated epidermal giant cells. In addition, not only the direct fluorescent absorption studies, but also the viral cultures were negative for both herpes zoster virus and herpes simplex virus. The bacterial culture from a crusted erosion was positive for methicillin susceptible S. aureus; the bacteria was also susceptible to cefazolin.

Discussion

Non-bullous impetigo is caused by either S. aureus or Streptococcus pyogenes. It typically presents as a superficial ulcer covered by a purulent exudate that dries into an adherent yellow to honey-colored crust. Lesions are frequently found on the face and extremities. Satellite lesions are common, resulting from self-inoculation [1,4-6].

Herpes zoster occurs when there is reactivation of a latent varicella-zoster infection. Skin lesions typically present as unilateral, erythematous-based vesicles in a dermatomal distribution. Less commonly, disseminated herpes zoster can present as multiple, widely distributed, individual vesicles—with or without—associated dermatomal skin involvement. In addition to a positive viral culture for varicella-zoster virus, bacterial culture can concurrently be positive for S. aureus when the vesicular, ulcerated or crusted lesions become colonized or secondarily infected by the bacterial organism [2,7-9].

Zosteriform impetigo represents the development of nonbullous impetigo, to date caused by S. aureus infection, in which the cutaneous lesions appear in a dermatomal distribution. Varicella-zoster virus is absent from the bacterial skin lesions. In addition to the reported patient, zosteriform S. aureus cutaneous infection has been described in 3 other individuals (Table 1) [3,10-13]; however, one might speculate that zosteriform cutaneous staphylococcal infection is probably more common than the paucity of reported individuals would suggest.

Table 1. Characteristics of patients with zosteriform cutaneous staphylococcal infections [a,b] [Copyright: ©2015 Cohen.]

There were 3 men and 1 girl; the latter was 17 years old. The men ranged in age from 63 to 76 years; the median age was 66 years. Dermatomes were affected equally on the right and left side of the body; two of the men had involvement of the same area: the facial skin innervated by the mandibular branch of the trigeminal nerve. The infection presented with clinical features of furunculosis (2 patients), impetigo (1 patient) or both (1 patient). Bacterial cultures of the skin lesion were positive for either methicillin-susceptible (2 patients) or methicillin-resistant (1 patient) S. aureus [14]. Viral culture, at this time of S. aureus infection, was negative for varicella-zoster virus; in addition, 3 of the 4 patients did not have a history of clinically significant herpes zoster (either in the affected area or elsewhere on their body). The bacterial infection was successfully treated with oral antibiotic in all patients; however one man experienced 2 recurrences in the same area.

Wolf’s isotopic response designates the occurrence of a new cutaneous disorder at the location of a previously healed skin disease [15]. It was originally termed “isoloci response” by Wolf and Wolf in 1985 [16]. A decade later, Ruocco suggested changing the name to “isotopic response” [10,17,18]. However, since the latter designation generated hundreds of references linked with radioactive isotopes during computer-obtained literature searches, it was subsequently changed to “Wolf’s isotopic response” [19].

Several types of postherpetic isotopic responses have been observed following either herpes simplex virus or varicella-zoster virus infections. These not only include fungal and other viral infections, but also acneiform lesions, dysimmune reactions, granulomatous reactions, leukemia and lymphomatous infiltrates, malignant tumors and other conditions [3,11,12]. Bacterial infections, such as furunculosis and S. aureus-associated nonbullous impetigo have each only been observed in 4 individuals (Table 1) [3,10-13].

A cutaneous immunocompromised district is an area of skin that—for either genetic or acquired reasons—is more vulnerable than the rest of the individual’s body. This vulnerable site often facilitates the onset of skin disorders or immunity-related eruptions at that area because of the local dysregulation of immune control. The immunocompromised district in dermatology is a designation that is intended to include all possible etiologies potentially involved in a local immune destabilization of the affected area of mucosa or skin [20,21].

Zosteriform impetigo is favored to represent Wolf’s postherpetic isotopic response in a cutaneous immunocompromised district [3,8,11,12]. The absence of a definitive history of preceding varicella-zoster virus infection in 75 percent of the individuals (3 of the 4 patients) may reflect a prior subclinical varicella-zoster virus infection, such as an episode of asymptomatic zoster sine herpete [7,8]. Alternatively, and often similar in presentation with a dermatomal distribution, is the possibility of a Blascho linear arrangement due to skin mosaicism [22].

Conclusion

Impetigo and herpes zoster are common bacterial and viral infections, respectively. Concurrent S. aureus infection or impetinization of varicella-zoster virus infectious skin lesions may occur; however, cultures of the skin lesions are typically positive for both bacteria and virus. However, similar to the described patient, the skin lesions of zosteriform impetigo are only culture positive for S. aureus; viral studies—including Tzanck smear, culture, direct fluorescent absorption, and polymerase chain reaction—are negative. Wolf’s isotopic postherpetic response in a cutaneous immunocompromised district is not uncommon; however, bacterial infection is seldom reported in this setting. Some of individuals with zosteriform cutaneous staphylococcal infections did not recall a prior herpes zoster infection at that site raising the possibility that they had previously experienced an episode of asymptomatic zoster sine herpete. Similar to non-dermatomal S. aureus infection, zosteriform impetigo promptly responded to antibiotics to which the bacteria are susceptible.

References

1. Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol 1994;11:293-303.

2. Kawai K, Gebremeskel BG, Acosta CJ. Systematic review of incidience and complications of herpes zoster: towards a global perspective. BMJ Open 2014;4:e004833. CrossRef

3. Ruocco V, Ruocco E, Ghersetich I, Bianchi B, Lotti T. Isotopic response after herpesvirus infection: an update. J Am Acad Dermatol 2002;46:90-4.

4. Hartman-Adams H, Banvard C, Juckett G. Impetigo: diagnosis and treatment. Am Fam Physician 2014;90:229-35.

5. Pereira LB. Impetigo-review. An Bras Dermatol 2014;89:293-9. CrossRef

6. Bangert S, Levy M, Hebert AA. Bacterial resistance and impetigo treatment trends: a review. Pediatr Dermatol 2012;29:243-8. CrossRef

7. Gilden D, Nagel MA, Cohrs RJ. Varicella-zoster. Handb Clin Neurol 2014;123:265-83. CrossRef

8. Staikov I, Neykov N, Marinovic B, Lipozencic J, Tsankov N. Herpes zoster as a systemic disease. Clin Dermatol 2014;32:424-9. CrossRef

9. Kim SR, Khan F, Ramirez-Fort MK, Downing C, Tyring SK. Varicella zoster: an update on current treatment options and future perspectives. Expert Opin Pharmacother 2014;15:61-71. CrossRef

10. Wolf R, Brenner S, Ruocco V, Filioli FG. Isotopic response. Int J Dermatol 1995;34:341-8.

11. Ruocco V, Brunetti G, Puca RV, Ruocco E. The immunocompromised district: a unifying concept for lymphoedematous, herpes-infected and otherwise damaged sites. J Eur Acad Dermatol Venereol 2008;23:1364-73. CrossRef

12. Ruocco V, Ruocco E, Brunetti G, et al. Wolf’s post-herpetic isotopic response: infections, tumors, and immune disorders arising on the site of healed herpetic infection. Clin Dermatol 2014;32:561-8. CrossRef

13. Schepp ED, Cohen PR. Zosteriform Staphylococcus aureus cutaneous infection: report of two patients with dermatomal bacterial infection. SkinMed 2015;13:275-81.

14. Cohen PR. Community-acquired methicillin-resistant Staphylococcus aureus skin infections: a review of epidemiology, clinical features, management, and prevention. Int J Dermatol 2007;46:1-11. CrossRef

15. Wolf R, Wolf D, Ruocco V, Ruocco E. Wolf’s isotopic response: the first attempt to introduce the concept of vulnerable areas in dermatology. Clin Dermatol 2014;12:557-60. CrossRef

16. Wolf R, Wolf D. Tinea in a site of healed herpes zoster (isoloci response?) [Letter]. Int J Dermatol 1985;24:539.

17. Wolf R, Ruocco V, Filioli FG. Isotopic response [letter]. Br J Dermatol 1997;136:466-7.

18. Wolf R, Lotti T, Ruocco V. Isomorphic versus isotopic response: data and hypotheses. J Eur Acad Dermatol Venereol 2003;17:123-5. CrossRef

19. Wolf R, Wolf D, Ruocco E, Brunetti G, Ruocco V. Wolf’s isotopic response. Clin Dermatol 2011;29:237-240. CrossRef

20. Ruocco V. The immunocompromised district: how the pieces of the puzzle gradually fell into place [commentary]. Clin Dermatol 2014;32:549-552. CrossRef

21. Ruocco V, Ruocco E, Piccolo V, et al. The immunocomporomised district in dermatology: a unifying pathogenic view of the regional immune dysregulation. Clin Dermatol 2014;32:569-76. CrossRef

22. Ruocco V, Ruocco E, Brunetti G, Saniuliano S, Wolf R. Opportunistic localization of skin lesions on vulnerable areas. Clin Dermatol 2011;29:483-8. CrossRef