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Clinical manifestations of varicella-zoster virus infection: Herpes zoster
Last literature review version 18.3: September 2010 | This topic last updated: September 23, 2010 (More)

INTRODUCTION — Varicella-zoster virus (VZV) infection causes two clinically distinct forms of disease. Primary infection with VZV results in varicella (chickenpox), characterized by vesicular lesions in different stages of development on the face, trunk, and extremities. Herpes zoster, also known as shingles, results from reactivation of endogenous latent VZV infection within the sensory ganglia. This clinical form of the disease is characterized by a painful, unilateral vesicular eruption, which usually occurs in a restricted dermatomal distribution.

This topic will address the clinical manifestations and complications of herpes zoster in immunocompetent and immunosuppressed hosts. The epidemiology, pathogenesis, diagnosis, and treatment of shingles, and the clinical manifestations of chickenpox are discussed elsewhere. (See "Epidemiology and pathogenesis of varicella-zoster virus infection: Herpes zoster" and "Treatment of herpes zoster" and "Diagnosis of varicella-zoster virus infection" and "Clinical features of varicella-zoster virus infection: Chickenpox".)

CLINICAL MANIFESTATIONS — The presenting clinical manifestations of herpes zoster are usually characterized by rash and acute neuritis.

Rash — The rash of herpes zoster starts as erythematous papules, which quickly evolve into grouped vesicles or bullae. Within three to four days, these vesicular lesions can become more pustular or occasionally hemorrhagic (picture 1 and picture 2). In immunocompetent hosts, the lesions crust by 7 to 10 days and are no longer considered infectious. The development of new lesions more than a week after presentation should raise concerns regarding possible underlying immunodeficiency [1]. Scarring and hypo- or hyperpigmentation may persist months to years after herpes zoster infection has resolved [2].

Zoster is generally limited to one dermatome in previously healthy hosts, but can occasionally affect two or three neighboring dermatomes (figure 1 and figure 2). Some patients have a few scattered vesicles located at some distance away from the involved dermatome [1,3].

The thoracic and lumbar dermatomes are the most commonly involved sites of herpes zoster (figure 1) [4]. A more serious infection, such as zoster keratitis or zoster ophthalmicus, can result from involvement of the ophthalmic branch of the trigeminal cranial nerve [2,5]. These can be sight-threatening infections. (See 'Complications in immunocompetent patients' below.)

Fewer than 20 percent of patients have significant systemic symptoms, such as headache, fever, malaise, or fatigue [1].

Acute neuritis — Pain is the most common symptom of zoster [6]; approximately 75 percent of patients have prodromal pain in the dermatome where the rash subsequently appears [1]. Prodromal pain may be constant or intermittent and can precede the rash by days to weeks [7]. Most patients describe a deep "burning", "throbbing", or "stabbing" sensation [7]. Some individuals describe the pain only when the involved area is touched, whereas others complain primarily of pruritus [8]. Pain that is induced by simple mild brushing against the skin is referred to as "allodynia".

In the absence of vesicular rash, certain pain syndromes can be confused with other etiologies, such as angina, cholecystitis, or renal colic, depending on the involved dermatome [4,9]. In one study of 1669 patients with confirmed herpes zoster, 18 percent had acute neuritis for at least 30 days and the duration of pain increased with age [4].

Atypical pain without rash — The concept that atypical pain syndromes may be related to herpes zoster without rash, or "zoster sine herpete", has been raised. Some clinical data showing serologic and PCR evidence of concurrent VZV reactivation have supported this theory [10].

CLINICAL RECURRENCES — Recurrence of clinical zoster in the immunocompetent host is rare [11]. However, recurrences do occur in the immunocompromised host [12]. In one study of HIV-infected patients, two hundred eighty-two episodes of herpes zoster were identified in 239 patients. Of these episodes, 158 were new occurrences of zoster and 124 were recurrent zoster events [12].


Overview — The most common complication of herpes zoster is postherpetic neuralgia. In one study, the percentage of patients with herpes zoster who developed postherpetic neuralgia (defined as at least 90 days of documented pain) increased from 5 percent in those younger than 60 years to 20 percent in those aged 80 years or older [13]. A randomized placebo-controlled trial in more than 38,000 adults demonstrated that zoster vaccine in the elderly reduces the incidence of PHN following zoster by 67 percent [14]. (See "Prevention of varicella-zoster virus infection: Herpes zoster".)

Other complications include ocular, neurologic, bacterial superinfection of the skin, which can delay healing of the zoster lesions [2,5,15,16]. (See "Postherpetic neuralgia".) Herpes zoster is not always limited to a spinal nerve distribution, but may also extend centrally, which can result in meningeal inflammation and clinical meningitis. Occasionally, VZV reactivation affects motor neurons in the spinal cord and brainstem, resulting in motor neuropathies [2,3,5].

Incidence of complications — In a review of 859 patients with herpes zoster, 100 patients (12 percent) developed 123 complications within 60 days [5]. A single complication occurred in 83 percent, two in 12 percent, and three or more in 5 percent. The risks of specific complications at 60 days were:

  • Postherpetic neuralgia — 7.9 percent
  • Bacterial skin infection — 2.3 percent
  • Ocular complications including uveitis and keratitis — 1.6 percent (see "Uveitis: Etiology; clinical manifestations; and diagnosis")
  • Motor neuropathy — 0.9 percent
  • Meningitis — 0.5 percent
  • Herpes zoster oticus — 0.2 percent

Twenty-seven percent of patients with complications had ophthalmic (trigeminal) zoster compared to the group of patients without complications in whom only 5 percent had this dermatome involved. Advanced age was associated with postherpetic neuralgia, bacterial superinfection of the skin, ocular complications, and motor neuropathy. Patients with one or more complications had more frequent comorbidities (eg, diabetes, cancer, HIV, transplant recipient).

Postherpetic neuralgia — Approximately 10 to 15 percent of all patients with herpes zoster will develop postherpetic neuralgia (PHN) [17]; individuals older than 60 years account for 50 percent of these cases [18]. PHN refers to pain persisting beyond four months from the initial onset of the rash. Sensory symptoms can include pain, numbness, dysesthesias, and allodynia (pain precipitated by movement) in the affected dermatome. Immunosuppressed patients have a higher incidence of PHN.

This topic is discussed in detail elsewhere. (See "Postherpetic neuralgia".)

Herpes zoster ophthalmicus — Herpes zoster ophthalmicus (HZO), a serious sight-threatening condition, has been linked to VZV reactivation within the trigeminal ganglion [19,20]. Incidence rates of HZO complicating herpes zoster in various population surveys have ranged from 8 to 56 percent [19,21]. The frontal branch within the first division of the trigeminal nerve is most frequently involved, and 50 to 72 percent of patients experience direct ocular involvement [19].

The acute syndrome typically begins with a prodrome of headache, malaise, and fever; unilateral pain or hypesthesia in the affected eye, forehead, and top of the head may precede or follow the prodrome. With the onset of a vesicular eruption along the trigeminal dermatome, hyperemic conjunctivitis, episcleritis, and lid droop can occur (picture 3) [15,19,20]. Almost two-thirds of HZO patients develop corneal involvement (keratitis) that results from a necrotic ganglionitis [19]; epithelial keratitis may feature punctate or dendriform lesions. Iritis occurs in approximately 40 percent of patients with herpes zoster ophthalmicus and can be associated with chronic vasculitis, atrophy, and poorly reactive pupils [19].

Clinicians should also be aware that vesicular lesions on the nose are associated with a high risk of herpes zoster ophthalmicus (Hutchinson's sign) [22]. Lesions in this area of the face signify involvement of the nasociliary branch of the trigeminal nerve, which also innervates the globe [23].

Early diagnosis is critical to prevent progressive corneal involvement and potential loss of vision [24]. The standard approach to herpes zoster ophthalmicus is to initiate antiviral therapy (acyclovir, valacyclovir, or famciclovir) to limit VZV replication and to use adjunctive topical steroid drops to reduce the inflammatory response and control immune keratitis and iritis [19,20,24,25]. Selected surgical procedures including corneal transplant and lid repair are performed less often.

Acute retinal necrosis (ARN) — VZV has been implicated as the leading causative pathogen of acute retinal necrosis (ARN) [26]; HSV has occasionally also been identified as an etiologic agent [27-29] and has been described in patients with a history of herpes encephalitis [30]. In a study evaluating samples of aqueous humor, VZV DNA was detected in seven of the nine patients with necrotizing retinopathies of suspected viral origin and in four of six patients with ARN [31]. (See "Retinal vasculitis associated with systemic disorders and infections".)

ARN in the immunocompetent host — ARN has been reported in immunocompetent hosts [31,32]. The clinical presentation features acute iridocyclitis, vitritis, necrotizing retinitis, occlusive retinal vasculitis with rapid loss of vision, and eventual retinal detachment [15,27,31,32]. Patients typically complain of blurred vision and pain in the affected eye due to progressive necrotizing retinitis; the disease can subsequently involve the other eye in 33 to 50 percent of patients [27]. The mechanism of bilateral involvement is not clear, but one study found a diminished or absent VZV-specific delayed hypersensitivity reaction in patients with ARN compared to patients with herpes zoster involving only the skin [33]. Retinal detachment is a common complication of ARN [26,34].

Intravenous acyclovir therapy for ARN usually affords clinical improvement in 48 to 72 hours [34] and can decrease the risk of contralateral eye involvement when administered for more than three months [31]. One pharmacokinetic study evaluated intravitreal drug concentrations in 10 patients with ARN after 24 hours of oral valacyclovir and found substantial penetration, even in the uninflamed eye [35]. Some practitioners use oral antiviral agents for maintenance therapy, although there does not appear to be a consensus on the need for long-term treatment [29]. There are few data on the use of oral agents for the initial treatment of infection [36].

Systemic corticosteroid use may decrease the severity of ocular inflammation [26].

ARN in HIV-infected patients — In patients with advanced AIDS and ARN, the following observations have been reported in the early era of potent ART [34]:

  • Rapid progression was characteristic; only 4 of 20 involved eyes retained useful vision at two-month follow-up, and 70 percent had no light perception at the conclusion of the study.
  • Eighty-two percent of patients had bilateral eye involvement; 70 percent sustained retinal detachment.
  • Seventy-three percent of patients had accompanying central nervous system (CNS) disease presumably due to VZV virus.

There are few data in the past decade regarding the management of this syndrome, which may be related to a decreased incidence of ARN in the era of potent HIV therapy. In one 2007 case report, aggressive antiviral therapy with intravitreal injections, initiation of ART, and serial sampling of vitreous for evidence of viral replication led to a good clinical outcome in the setting of immune reconstitution [37].

Ramsay Hunt syndrome (Herpes zoster oticus) — The major otologic complication of VZV reactivation is the Ramsay Hunt syndrome, which typically includes the triad of ipsilateral facial paralysis, ear pain, and vesicles in the auditory canal and auricle [38,39]. Taste perception, hearing (tinnitus, hyperacusis), and lacrimation are affected in selected patients [39]. Ramsay Hunt syndrome is generally considered a polycranial neuropathy with frequent involvement of cranial nerves V, IX, and X [38]. Vestibular disturbances (vertigo) are also frequently reported. Ramsay Hunt syndrome has also been reported in association with herpes simplex type 2 infection [40].

Ramsay Hunt syndrome has been linked to reactivation of latent VZV residing within the geniculate ganglion [41] with subsequent spread of the inflammatory process to involve the eighth cranial nerve. This results in auditory and vestibular disorders [42]. VZV DNA has been detected in 11 of 14 trigeminal ganglia (79 percent) and in 9 of 13 geniculate ganglia (69 percent) in adults but was not isolated from any newborn ganglia specimens or from one adult seronegative for VZV [42]. These results indicate that VZV becomes latent in the human geniculate ganglion after primary varicella infection, and reactivation of VZV from the geniculate ganglion most likely precipitates the Ramsay Hunt syndrome [42].

The facial paralysis seen in Ramsay Hunt syndrome is felt generally to be more severe than Bell's palsy attributed to HSV, with increased rates of late neural denervation and a decreased probability of complete recovery [43,44]. Antiviral therapy is usually prescribed, although there are few data on this complication and management [45].

Other neurologic complications

Aseptic meningitis — Several studies conducted in patients with herpes zoster have demonstrated that subclinical meningeal irritation, evidenced by a reactive cerebrospinal fluid (CSF) pleocytosis, can occur in 40 to 50 percent of cases [46,47]. A subset of immunocompetent patients with herpes zoster develop clinically evident aseptic meningitis [48]; lumbar puncture typically confirms a brisk CSF pleocytosis and an elevated protein concentration [49,50]. In a Finnish epidemiologic study of 144 patients with aseptic meningitis, an etiology was established in 66 percent of patients, 8 percent of whom had VZV infection [48].

Peripheral motor neuropathy — Segmental motor paresis develops in approximately 3 percent of patients with zoster [46,51]. Peripheral motor weakness is felt to result from spread of VZV from the dorsal root ganglia to the anterior root/horn; the onset is typically coincident with the development of pain and cutaneous eruption in a dermatomal distribution [46,51,52]. Muscle atrophy may result in the affected region, but approximately 75 percent of patients experience gradual recovery of motor strength [46].

Myelitis — Transverse myelitis occasionally complicates herpes zoster (usually involving thoracic dermatomes (figure 1)) within days to weeks following the initial onset of the vesicular rash [46,53]. Myelitis is a more frequent complication in HIV-infected patients and involves direct spread of VZV from the dorsal root ganglia centrally into the spinal cord [54,55]. Several reports describing zoster myelitis in HIV-infected patients in the absence of any rash have documented VZV DNA within spinal cord specimens at autopsy [54].

Encephalitis — Zoster-associated encephalitis typically presents with delirium within days following the vesicular eruption but may occur prior to the onset of rash or follow an episode of zoster by more than six months [46,56]. While apparently normal hosts may develop VZV encephalitis, the majority of cases have been reported in immunosuppressed patients, such as HIV-infected individuals [15,46,56-58]. Major risk factors identified for the development of zoster encephalitis include cranial or cervical dermatomal involvement, two or more prior episodes of zoster, disseminated herpes zoster, and impaired cell-mediated immunity [46,57].

AIDS patients may develop a leukoencephalitis associated with CNS white matter demyelination and cerebral vasculopathy due to ongoing VZV replication within the brain parenchyma [46,59]. Response to acyclovir therapy in AIDS patients has been variable due to the frequent emergence of acyclovir-resistant VZV strains during long-term exposure to the drug [60-62]. CSF PCR assays, in conjunction with MRI brain imaging studies, have facilitated more rapid diagnosis of VZV-induced encephalitis in selected patients [63,64].

Guillain-Barre syndrome — Data from a Taiwan health registry was extracted to determine if there was an increased risk of Guillain-Barré Syndrome (GBS) among those with a history of herpes zoster within the prior two months of presentation [65]. Of 315,595 patients with a history of herpes zoster, 0.03 percent developed GBS. Although GBS was a relatively rare event, the risk of developing this syndrome was significantly higher among patients with a recent history of zoster compared with controls, who were matched by age and sex. (See "Clinical features and diagnosis of Guillain-Barré syndrome in adults".)

Stroke syndromes — VZV infection can produce stroke syndromes secondary to infection of cerebral arteries. In a series of 30 patients with VZV vasculopathy, diagnosed by either VZV-specific antibodies or VZV DNA in the CSF, rash occurred in 19 (63 percent) and CSF pleocytocytosis in 20 (67 percent) [66]. Angiography demonstrated the involvement of both large and small arteries in approximately half of the patients. (See "Stroke caused by varicella zoster virus".)

The pathogenesis of stroke following an episode of dermatomal zoster has been linked to direct viral invasion of cerebral arteries with VZV by extension along the intracranial branches of the trigeminal nerves resulting in an inflammatory process within the internal carotid artery or its branches on the side ipsilateral to the rash [15,67].

Granulomatous vasculitis of the large and small arteries, with VZV antigens detectable in the smooth muscle cells of the media, has been confirmed in several autopsy studies [68]. These pathologic findings have suggested that the syndrome results from direct VZV invasion of the arterial surface via spread along the intracranial branches of the trigeminal nerve [46,68]. The mortality rate is at least 20 percent, and survivors have severe neurologic deficits [46].

HZO has rarely been complicated by contralateral thrombotic stroke syndrome in some patients [46,68,69]. (See "Stroke caused by varicella zoster virus".) This catastrophic syndrome typically occurs within several weeks to a few months after the zoster eruption [46] and is heralded by the abrupt onset of severe headache and rapid evolution to contralateral motor weakness. Cerebral angiography demonstrates multifocal occlusion of the proximal branches of the anterior and middle cerebral arteries [70].

COMPLICATIONS IN IMMUNOCOMPROMISED HOSTS — Immunocompromised hosts, including both HIV-infected patients and transplant recipients, remain at substantial risk for severe VZV-related complications [15,46,54,55,71-74].

Disseminated VZV has been documented in both solid organ transplant recipients and in patients with hematologic malignancies undergoing chemotherapy [72,75,76]. Cutaneous dissemination is often accompanied by visceral involvement [76,77]. Visceral dissemination in the immunosuppressed transplant patient is a life-threatening emergency [78]. In transplant patients, reactivation of VZV typically occurs later than CMV or HSV [79]. Cutaneous lesions may be delayed, or atypical with hemorrhage [78].

VZV pneumonitis in transplant recipients has been associated with a high mortality despite prompt diagnosis and the empiric institution of antiviral therapy [80].

Bone marrow transplant recipients — VZV dissemination remains the most frequent late infection of allogeneic bone marrow transplant (BMT) recipients [75,76]; concurrent graft versus host disease (GVHD) has been identified as a major risk factor for dissemination [76]. (See "Overview of infections following hematopoietic cell transplantation".) Infection with reactivated VZV occurs in 35 percent of allogeneic BMT recipients at one year; almost 50 percent of these patients will develop disseminated VZV [81]. Visceral VZV dissemination can be accompanied by pneumonitis, hepatitis, pancreatitis, and/or meningoencephalitis [73,74].

Selected BMT recipients have presented with acute, severe abdominal pain as the initial manifestation of visceral reactivated VZV in the absence of antecedent cutaneous rash, hepatitis, or pneumonitis [75,82]. The appearance of a zoster rash as long as 10 to 14 days after abdominal pain begins has frequently delayed prompt diagnosis and resulted in a poor outcome despite the institution of appropriate antiviral therapy.

HIV-infected patients — HIV-infected patients are at increased risk of developing herpes zoster than the general population and are at increased risk of neurologic and ophthalmologic complications [15].

The incidence and clinical spectrum of herpes zoster was evaluated in an urban clinic of HIV-infected patients; 52 episodes of zoster occurred in 45 patients during 1614 person-years of follow-up (incidence, 3.2 episodes per 100 person-years) [71]. In this study conducted in the pre-HAART era, low CD4 count was associated with zoster-related complications, such as retinal necrosis and aseptic meningitis.

One retrospective study evaluated VZV infections before and after the introduction of potent ART [83]. The incidence of HZ in the pre-HAART era (17 per 100 person years) was significantly higher than that in the post-HAART era (5 per 100 person-years). Furthermore, in both eras, the incidence of HZ was higher in the first six months after initiating ART than between 6 and 12 months. Another retrospective study with a case-control design determined that 18 percent of patients who had herpes zoster developed PHN [12].

Reactivation of herpes zoster has also been reported as part of the immune reconstitution inflammatory syndrome [84-86]. This topic is discussed in detail elsewhere. (See "Immune reconstitution inflammatory syndrome".)

DIAGNOSIS — Shingles is typically characterized in immunocompetent individuals by a unilateral vesicular eruption with a well-defined dermatomal distribution. The diagnosis is usually established based solely on the clinical presentation.

Shingles, however, may occasionally present with atypical skin lesions, especially in immunosuppressed individuals. Patients with recurrent HSV reactivation may develop vesicular lesions in an unusual distribution that are difficult to distinguish from a VZV eruption. In circumstances where the clinical presentation is uncertain, laboratory confirmation is indicated.

Diagnostic techniques include viral culture, direct immunofluorescence testing, and the polymerase chain reaction assay, which is the most sensitive test. These diagnostic assays are discussed elsewhere. (See "Diagnosis of varicella-zoster virus infection".)

DIFFERENTIAL DIAGNOSIS — Once the rash of herpes zoster has appeared, the diagnosis is usually readily apparent. The other main agent to consider in the differential diagnosis is herpes simplex. Herpes zoster is mainly characterized by a painful sensory prodrome, dermatomal distribution, and lack of prior history of a similar rash. If the patient has had a similar vesicular rash in the same location, then recurrent zosteriform herpes simplex should be considered. A non-infectious etiology to consider is contact dermatitis.

The immunocompromised host may present with atypical findings, such as nodular lesions or chronic crusting of the skin. Diagnostic laboratory testing should be utilized.

INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. (See "Patient information: Shingles".) We encourage you to print or e-mail this topic review, or to refer patients to our public web site,, which includes this and other topics.


  • The presenting clinical manifestations of herpes zoster are usually characterized by rash and acute neuritis. The thoracic and lumbar dermatomes are the most commonly involved sites of herpes zoster (figure 1). Immunocompromised hosts may develop disseminated lesions. (See 'Clinical manifestations' above.)
  • Recurrence of clinical zoster in the immunocompetent host is rare, but does occur in the immunosuppressed host. (See 'Clinical recurrences' above.)
  • The most common complication of herpes zoster is postherpetic neuralgia. Other complications include herpes zoster ophthalmicus or oticus, acute retinal necrosis, aseptic meningitis, and encephalitis. (See 'Complications in immunocompetent patients' above.)
  • Immunocompromised hosts are at risk for cutaneous and visceral dissemination. (See 'Complications in immunocompromised hosts' above.)
  • The diagnosis is usually made clinically; available diagnostic techniques include viral culture, direct fluorescent antibody testing, and the polymerase chain reaction assay. (See "Diagnosis of varicella-zoster virus infection".)
  • The principle other main infectious agent to consider in the differential diagnosis of vesicular lesions is herpes simplex. (See 'Differential diagnosis' above.)
  • Educational materials on this topic are available for patients. (See "Patient information: Shingles".)
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