Dermatology Online Journal

Syringitis: A clue to herpes infection
Michael Paul Sedrak¹ MD, Michaela Marek² BS, Ryan Matherne³ MD, Brent Kelly³ MD
Dermatology Online Journal 18 (8): 6

1. Department of Pathology, University of Texas Medical Branch, Galveston, Texas
2. School of Medicine, University of Texas Medical Branch, Galveston, Texas
3. Department of Dermatology, University of Texas Medical Branch, Galveston, Texas

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Abstract

Herpes simplex virus (HSV) is a member of the herpes virus family that commonly affects the skin. Typical histopathologic findings are usually limited to the epidermis and include intraepidermal vesicles or ulceration and epidermal necrosis. More specific findings in herpes virus infection include enlarged and pale keratinocytes, with steel-gray nuclei and margination of chromatin at the edge of the nucleus and ballooning degeneration. Although histopathologic changes may occasionally involve the hair follicles or sebaceous glands, it is very rare to find HSV involving the eccrine glands. We present a case of a 13-month-old child with a large body burn diagnosed with HSV (in the absence of the epidermis) by the presence of syringitis with herpetic features in the absence of the epidermis to aid in diagnosis.

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Introduction

HSV can be diagnosed by finding certain histopathological features in the epidermis. Herein is a case of HSV diagnosed by the presence of syringitis accompanied by herpetic features in a thermal burn patient in which the epidermis was absent on the biopsy specimen.

Case report

Figure 1	Figure 2
Figure 1. Confluent annular ulcers of the scalp in areas of absent epidermis Figure 2. Annular ulcers on the leg in areas of absent epidermis

Figure 3	Figure 4
Figure 3. Ulcers in areas of absent epidermis on the arm and hand Figure 4. Tangential biopsy showing absent epidermis with ballooning degeneration of the eccrine ducts (H&E x40)

A 13-month-old female presented with a 90 percent BSA scald burn from heated water. She was taken to an outside hospital where she received initial burn resuscitation. Three days later the patient was transferred to Shriner’s Hospital in Galveston, Texas, where she underwent numerous excision and homografting procedures as routine treatment of these patients. After 3 weeks of treatment, the patient developed confluent vesicles and ulcerations in all areas involving the burn and grafting procedures (Figures 1, 2, and 3). Histopathologic examination at scanning magnification of the biopsy from one of the lesions showed complete absence of the epidermis with an inflammatory infiltrate in the syrinx. Closer examination revealed large cells lining the lumens of eccrine glands and ducts. These cells showed ballooning degeneration, molding of nuclei, and margination of chromatin. An accompanying acute infiltrate with neutrophilic dust was also present (Figures 4 and 5). HSV was suspected and confirmed with positive staining on immunohistochemical analysis (Figure 6). She received IV acyclovir but later lost all donor and graft sites. Additional excision and reapplication of homografting was attempted without success. The patient became ventilator dependent, developed bacteremia with highly resistant pseudomonas followed by septic shock, and died.

Figure 5	Figure 6
Figure 5. Ballooning degeneration of the eccrine ducts (H&E x100) Figure 6. Immunohistochemical staining for HSV highlighting multinucleated giant cells of the eccrine duct (x200)

Discussion

HSV is a highly contagious virus and is a member of the herpes viridae family, which includes Varicella Zoster Virus (VZV) and others. Of the viruses in this family, HSV and VZV classically involve the skin. HSV seropositivity is very common in the US and it is estimated that 58 percent of the US population is seropositive for HSV type 1 and 17 percent of the population seropositive for type 2 [1]. Clinical presentation of HSV is well known to dermatologists and typically includes vesicles, watery blisters in the mucocutaneous tissue involving the mouth, lips, or genitals. Lesions heal with a scab characteristic of herpetic disease. However, HSV-1 and -2 are neurotropic and neuroinvasive viruses and persist in the body by becoming latent in the cell bodies of nerves. After the initial or primary infection, HSV is notorious for viral reactivation or outbreaks, which can be life threatening especially if the host is immunocompromised. In an outbreak, the virus in a nerve cell becomes active and is transported via the nerve to the skin, where virus replication and shedding occur and cause new sores. The clinical features correlate well with some of the histopathologic features common to HSV: intraepidermal vesicles or ulceration and epidermal necrosis. Other, more specific, features of herpes involvement include enlarged and pale keratinocytes, with steel-gray nuclei and margination of chromatin at the edge of the nucleus, and ballooning degeneration. Histopathologic examination alone cannot differentiate between HSV and VZV making clinical presentation vital; ancillary studies such as PCR are necessary in unclear cases. It has been noted, however, that HSV changes usually are confined to the epidermis, whereas VZV can more commonly also involve the adnexa, although these generalizations are not absolute [2] as demonstrated in the present case. Because microscopic examination alone cannot differentiate between VZV and HSV, herpes will be used as a general term that includes these two viruses unless otherwise specified. HSV can infrequently involve the adnexa and can present as a folliculitis, which is an atypical clinical presentation and microscopic finding. Folliculitis has been cited as an under-appreciated presentation of viral infection so some have suggested that a viral etiology must be considered in a patient with folliculitis that is not responding to antibacterials and antifungals regardless of immune status [3, 4, 5].

It has been estimated that 8-25 percent of pediatric burn patients have evidence of HSV infection [6] and it may be particularly difficult to clinch a diagnosis of herpes infection in these patients with a preexisting erosive wound [7] because a lesion may not demonstrate the grouped vesicular pattern of scalloped edges. Lesions caused by HSV can present as a hemorrhagic or purpuric rash, papules, papulovesicles, pustules, or confluent vesicles creating larger areas of ulceration [8].

Burn victims may have epidermal necrosis related to advanced herpetic disease or directly from the burn, which complicates the dermatopathogist’s job of ruling out HSV in an ulcerated lesion because HSV most commonly affects the epidermis. Unfortunately, the underlying condition that increases the likelihood for atypical presentation (e.g., immunocompromised patients having advanced disease or burn patients who have epidermal damage from the burn), also necessitates prompt diagnosis and treatment in these high risk patients.

Involvement limited to adnexa may be a clue to herpes infection in patients who are immunocompromised [9, 10]. Our case is an example of how syringitis can serve as a clue of herpes infection in a burn patient with absence of epidermis. Herpetic involvement of the eccrine glands may reflect the profound depression of cellular immunity [9]. It is of note that both epidermal and eccrine duct involvement have been present together in other cases [11, 12]. There has been one case, to our knowledge, in which herpetic syringitis was present in an immunocompetent patient [5].

Our report suggests that syringitis may be an underappreciated sign of active herpes infection, especially in immunocompromised patients who may have loss of the epidermis. More careful search for the classic histopathologic findings of herpes infection in the presence of syringitis is warranted in these vulnerable patients.

References

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