Vibrio vulnificus necrotizing fasciitis preceding herpes zoster

Abstract

A 74-year-old white man presented with unilateral radicular pain extending across the left side of his chest and back. A diagnosis of postherpetic neuralgia, a sequela of herpes zoster, was made. Herpes zoster represents a reactivation of the varicella zoster virus that lies dormant in patients with past chickenpox. Risk factors for the disease include advanced age, stress, immunodeficiency, and immunosuppression. Treatment of herpes zoster entails traditional antiviral medications, while prevention may be achieved with a new prophylactic vaccine.

Herpes zoster (HZ), also known as varicella zoster or more colloquially as “shingles,” is a neurodermal disease characterized by unilateral radicular pain, tingling, pruritus, and a characteristic vesicular rash set on an erythematous base. The rash entails a reactivation of the latent varicella zoster virus (VZV) that lies dormant in cranial or sensory nerve ganglia. The most commonly affected dermatomes lie in the cranial and thoracic regions of the body. Approximately 98% of the population remains susceptible to HZ, as the virus lies quiescent in individuals previously afflicted with chickenpox. Because of such widespread susceptibility, it is important to identify the risk factors that may predispose one to HZ.

CASE REPORT

A 74-year-old white man presented with a 10-month history of unilateral radicular pain extending across the left side of his chest and back in the region of the T5 dermatome; he rated this pain as a “10” on a 0- to 10-point scale. The patient revealed that his HZ outbreak had been preceded by necrotizing fasciitis, which resulted in several hemorrhagic bullae located along the left upper extremity (C6, C7, and C8) (Figure 1). The infection was induced by a puncture wound that arose while the patient was fishing in the Gulf of Mexico. He was hospitalized for 1 week and treated with cefotaxime, ciprofloxacin, and minocycline. Approximately 7 days following his discharge from the hospital, the hemorrhagic bullae had begun to resolve and painful vesicles in the adjacent T5 dermatome began to emerge. The patient was subsequently diagnosed with HZ and treated with famciclovir. Previously, he had type 2 diabetes mellitus treated with rosiglitazone.

Figure 1.

Necrotizing fasciitis along the left C6, C7, and C8 dermatomes induced by a puncture wound while the patient was fishing in the Gulf of Mexico.

Examination revealed a hypopigmented scar that closely followed the course of pain along the indicated dermatome (Figure 2). Swelling and soreness were noted under the patient's left arm, making any voluntary movement of the arm extremely painful. Though the patient did not have a history of shingles, he affirmed that his son, grandson, and brother had all been afflicted with the malady at various times. The patient remembered having had chickenpox as a child.

Figure 2.

Hypopigmented scar from herpes zoster present on the left side of the patient's body in the region of the T5 dermatome.

DISCUSSION

Although most of the population remains susceptible to HZ after recovering from a bout of chickenpox, the lifetime risk is estimated at approximately 15% (1). This incidence, however, rises dramatically with age, affecting up to 50% of those ≥85 years. Advanced age represents the most potent risk factor for the development of HZ and its associated sequelae. Among these sequelae are postherpetic neuralgia (PHN), ophthalmic zoster, Ramsay-Hunt syndrome, bacterial superinfection, scarring, meningoencephalitis, pneumonitis, and hepatitis (2). PHN is the most serious complication and is characterized by chronic HZ-associated pain that lingers for months to years after the erythematous rash has disappeared (1). The increased risk of HZ among the elderly may result from a general waning of cellular immunity that occurs with advanced age. Alternatively, a prolonged length of time since primary varicella exposure may contribute to a heightened risk for HZ (3). The age at which the most dramatic rise in HZ incidence occurs is about 60 years. Patients with HIV/AIDS, certain cancers, organ transplants, and those receiving immunosuppressive treatments have also been shown to have a heightened risk for HZ (4).

Aside from aging and immunosuppression, a number of additional risk factors may contribute to the prevalence of HZ. Stress, both psychological and mechanical, appears to play an important role in the attainment of the disease. Trauma, surgery, and/or injury to a specified region of the body may induce or predispose one to an outbreak of HZ. Nerve stimulation from mechanical trauma may precipitate HZ in the affected dermatome by triggering reactivation of the virus in the dorsal root ganglion (4).

Vibrio species may affect humans through three clinically distinct illnesses: gastroenteritis, wound infection, and primary septicemia. Infection may arise when chafed skin or minor abrasions are exposed to seawater or during the preparation of seafood (5). Alternatively, penetrating injury by fish fin spines or ingestion of uncooked seafood may ultimately result in soft tissue infections and lethal septicemia. Injury to the distal extremities caused by fish fin spines is frequently sustained by fishermen and those who handle live seafood (6).

Vibrio vulnificus is a naturally occurring, Gram-negative, halophilic bacterium found in both estuarine and marine environments throughout the world. Its presence is especially prevalent within the warm coastal waters of the Gulf of Mexico, South America, Asia, and Australia. Infection with V. vulnificus may lead to the development of necrotizing fasciitis and primary septicemia, two complications that are most prevalent in immunocompromised patients with underlying hepatic disease, diabetes mellitus, chronic renal insufficiency, and adrenal insufficiency (7). Our case report highlights the development of necrotizing fasciitis in a diabetic patient who acquired a puncture wound while fishing in the Gulf of Mexico. The trauma induced by the wound and its subsequent necrotizing fasciitis may have provided an adequate degree of stress to provoke the development of HZ and its associated PHN.

Although many of the predisposing factors to HZ are acquired throughout one's lifetime, others may be inherent. A recent study proposed that a distinct polymorphism in the promoter region of the interleukin-10 (IL-10) gene may be responsible for this genetic susceptibility, as IL-10 is a cytokine that aids in downregulating cellular immunity (8). In addition, an individual's ethnicity may play a role in the attainment of HZ. Previous studies (4, 9–11) have demonstrated a lower prevalence of HZ in black individuals as compared to white individuals. Hypothesized reasons for these disparities include differences in VZV immunity, age of varicella onset, and exposure to varicella over one's lifetime (12).

The clinical course of HZ often begins with a prodrome characterized by pain, paresthesias, general malaise, fever, and lymphadenopathy. Prodromal symptoms may last 1 to 3 days and occur in approximately 80% of HZ patients. Following the viral prodrome, a distinctive unilateral eruption of herpetiform vesicles occurs in one or more affected dermatomes. The HZ rash begins as erythema, followed by water-clear vesicles at 12 to 24 hours, confluent vesicles at 48 to 96 hours, and pustules at 72 hours. New crops of vesicles continue to emerge for 1 to 7 days. The cranial and thoracic regions of the body are most frequently affected (13), with <1% of patients exhibiting bilateral nerve involvement (14). Some patients may not develop the characteristic HZ rash, a condition termed “zoster sine herpete,” which may further complicate the diagnosis (15).

Early identification of HZ is crucial in the treatment and prevention of the virus's numerous complications. Diagnosis of HZ is often made by clinical observation alone. Three antiviral drugs, acyclovir, famciclovir, and valacyclovir, are currently available for the treatment of HZ and appear to be more effective than treatment with corticosteroids alone (15). Though acyclovir is significantly less expensive, famciclovir and valacyclovir are preferred due to more convenient dosing regimens (5 times daily versus 3 times daily, respectively). One study demonstrated that famciclovir could reduce acute HZ pain by 1 to 2 days and PHN pain by 60 days if given within 72 hours of an outbreak (16). Famciclovir has since been shown to be equivalent to valacyclovir in regards to rash healing time and reduction of pain caused by PHN (17).

A new vaccine that was approved by the Food and Drug Administration in May 2006 may be the best option for those at risk for HZ. In October 2006, the Centers for Disease Control and Prevention recommended Zostavax as part of a routine vaccination for senior citizens aged ≥60 years. A study highlighting the efficacy of Zostavax revealed that cases of HZ were reduced by half in those who received the vaccine versus placebo. Participants who were vaccinated but still acquired HZ were 66% less likely to develop PHN than those given a placebo (18). Hence, the new HZ vaccine may reduce the incidence of HZ and its potential complications in patients with a heightened risk of developing the disease.