Herpes zoster, clinical signs and therapy

Konrád, P. Dermatology Clinic in Černošice / Lasermed

SUMMARY: Shingles (herpes zoster) is an acute segmental disease with skin and neurological manifestations, usually typical of the clinical picture and course, which is caused by the varicella-zoster virus (VZV) of the herpesvirus group. It is an expression of reactivation of the virus, which persists in the sensitive ganglia of the human body after primoinfection with chickenpox. Reactivation occurs as a result of immunosuppression due to age, disease, immunosuppressive treatment or another stress factor. Since it is classified as precancerous, screening patients is recommended after shingles. The course of the diseases may be more severe in individuals with a compromised immune system and it may even be associated with serious to fatal complications. Due to the location of the process, the course of herpes zoster trigeminalis is accompanied by additional symptoms, the most serious of which may involve eye problems and extreme trigeminal pain. Inadequate or late onset of therapy results in postherpetic neuralgia. Due to the intensity and the fact that it may even last several months, they are very bothersome and debilitating. In older literature, shingles is even classified as a cause of suicide. Much progress has been made in the prevention of shingles in recent years. This article discusses the aetiology, clinical signs and current therapeutic recommendations.

KEYWORDS: shingles, clinical picture, treatment.


The Origin of the Name of the Disease

Herpeton means “to creep” in Greek – similar to the spread of individual efflorescence, which gradually intensifies and resembles a snake (Fig.1). Zoster means “belt” in Greek – similar to the striped-like rash. (1) Traditionally, a third word, which determines which dermatome was affected, is also used to name the disease.


Herpes zoster (shingles) is an acute segmental disease with skin and neurological clinical manifestations, usually typical of the clinical picture and course, which is caused by the varicella-zoster virus (VZV) of the herpesvirus group (Fig.2).


The disease was known of back in the Middle Ages. The discovery that the centre of the disease is located in the spinal ganglia was first described in 1848 by von Bärensprung, who called it the ganglionitis acuta posterior disease (1). The relationship between herpes zoster and varicella was clarified by the works of von Bokay in 1888 (published in 1909).  A bit later, Lipschütz confirmed that the histological picture of the skin lesions of herpes zoster and varicella are the same. In 1925, Kundratitz clarified the infectiousness of the disease. In 1906, American pathologist, Tyzzler, working in the Philippines, first described the identical histological picture of the skin manifestations of herpes zoster and varicella. Amiese clarified the serological relationship between herpes zoster and varicella in 1934 and the virus was first visualized in 1943. In 1958, Weller (Nobel Prize) (Fig. 3) succeeded in isolating the VZV on cell cultures. Davison and Scott clarified the genome of the VZV in 1986. In 1831, Richard Bright discovered the neurological changes in the segment with skin rashes of herpes zoster. Nealy thirty years later, in 1862, Barensprung described the inflammatory changes in the corresponding spinal ganglia. Esirini and Tomlison (2) were the first to report electron-microscopic and histological evidence of the VZV in sensory ganglia of the trigeminalis nerve in 1972.

Aetiology and Pathogenesis

Herpes zoster is one of the so-called herpetic diseases, so a disease caused by a large group of herpetic viruses. Herpetic viruses are DNA viruses. Their genome consists of a DNA molecule. They have a complex structure and belong to the largest known group of viral agents ever. After infecting the host, they have the ability to survive in its cells for a long time and under certain conditions, like the current state of the host’s immunity. However, other factors are also capable of reactivation. The primoinfection may also occur latently (ex. 1% to 95% in HSV, very rare in VZV) or with minimal atypical symptoms. The incubation period is 7-14 days. After the primary infection, the virus remains in the organism permanently. Human herpes viruses are classified into 3 sub-groups: Alpha herpes viruses: type 1 herpes simplex virus (HSV 1), type 2 genitals herpes simplex virus (HSV 2), varicella zoster virus (VZV), Beta herpes viruses: cytomegalovirus (CMV), type 6 human herpetic virus (HHV-6), type 7 human herpetic virus (HHV-7) and Gama herpes viruses: Epstein and Barr virus (EVB) and type 8 human herpetic virus (HHV-8). Of the selected human viruses: the alfa herpes viruses (HSV 1, HSV 2, virus varicella-zoster) and CMV of the beta herpes virus group are generally highly infectious. They are either transmitted by direct contact or by the respiratory route. They are very infectious agents. Worldwide, they are among the most wide-spread viral agents in the human population. Man is their only reservoir. (3)

Clinical Picture

The disease is preceded by a prodrome stage, which is characterized by fatigue, subfebrile, head ache and muscle pain, patients interestingly report nightmares before getting the rash. The patient experiences unpleasant changes in the sensitivity of the skin before the vesicles erupt. The patient also experiences a low or hyper-sensitivity to pressure, even clothes on the body. The pain may even sometimes by so distinct that it may imitate a migraine, heart pain, bladder or kidney stones, vertebrogenic algic syndrome or odontogenic pain. (4) Typical skin symptoms begin like erythematous macules, papules or plagues with herpes blisters aligning up on them within 12–24 hours (Fig.4). The blisters are arranged into groups of various sizes, but some may appear on their own (Fig.5). Their size ranges from a few milometers, the cover is initially tense and the centre gradually sinks in. The content is initially clear but gradually becomes cloudy. Once the blisters burst and the base is exposed, extensive watery, map-like lesions are formed (Fig.6). Once the deposits dry up, they turn into crusts. Once the crust separates, colour changes last a long time – this is called post-inflammatory pigmentation. The rash is gradual, so morphs of different stages of development are visible in the affected area. The course and clinical picture may somewhat differ from the “norm”. The difference may occur in the extent of occurrence, in the skin lesions, in the overall course and in other clinical signs. Herpes zoster multiplex may occur if more dermatomes are affected or the rare herpes zoster bilateralis, affecting both sides, may occur. A disseminated zoster variant may also occur in severely immunosuppressed individuals. There is also a so-called herpes zoster sine herpete, which is only manifested by various degrees of sensation and pain in the affected area, but without blisters. The blisters are filled with blood in herpes zoster haemorrhagicus. Herpes zoster gangrenous, with a gangrenous blister base may develop. In this case, the disease leaves scars. It occurs more often in individuals with more pronounced immunosuppression (5,6). The infection is severe in HIV/AIDS patients. It affects multiple dermatomes, extensive haemorrhagic lesions appear, the symptoms are slow to heal and organ disorders develop (encephalitis, keratitis, interstitial pneumonia). Other symptoms and consequences may result if shingles appear in the area of the head.

Herpes zoster ophthalmic, (I. branch of n. trigemini) is not only a rash on the skin but also the eye. It is accompanied by eye damage. It may affect all structures of the eye. The virus may cause inflammation of the front segment (conjunctiva, iris, cornea, sclera) and the back segment of the eye with impaired vision. Herpetic morph rashes on the tip of the nose are called Hutchinson’s marks and indicate a higher risk of damage to the eye structure. The symptoms include pronounced pain, swelling of the eyelids and watery eyes. When the patient suffers from n. nasociliaris (which is accompanied by the Hutchinson’s mark), it affects the structure of the eye, which may develop into ulcer keratitis, scleritis, uveitis, optic nerve lesions are rare, glaucoma, ptosis of the eyelid, scarring and even blindness. (6,7)

Herpes zoster maxillaris (II. branch of N. V) and mandibularis (III. branch of n. V) is not only associated with rashes on the skin, face, cheeks and chin but also on the mucous membrane of the oral cavity and tongue, with erosions and ulcerations and a rare development of severe gingivitis. Herpes zoster in the area of the facial nerve is oftentimes accompanied by vesicles in the external ear canal, otalgia, loss of taste in the frontal 2/3 of the tongue and it may also be associated with paresis of the facial nerve. Herpes zoster optic, with rashes in the area of the facial nerve (n. VII) and n. vestibulocochlearis (N. VIII), is known as the Ramsey Hunt Syndrome. These are deposits in the Ramsey Hunt sensitive zone area (the pinna, external ear canal, mastoideus process areas), affecting the outer, middle and inner ear and paresis of the facial nerve. Symptoms of the Ramsey Hunt Syndrome include otalgia, tinnitus, nystagmus, vertigo, hearing impairment, reduced production of saliva and tears. Herpes zoster larynges in the n. glossopharyngeal (n. IX) and n. vagus (n. X) affects the throat, tonsils and palate. (6,8) The rash is infectious even though it does not reach such level of infectiousness like varicella. Shingles may recur. (6,8)


Firstly, shingles is diagnosed om the basis of a clinical picture, which tends to be typical for the most part. The anamnesis usually includes information about a recent disease, stressful situation, increased physical strain (ex. after running a marathon), mental strain or trauma. Diagnostic difficulties may occur at the beginning, during the initial prodromal pains, which precede the rash and which may give rise to suspicions of somatic disease (ex. heart attack). Disseminated herpes has to be differentiated from other disseminated exanthem. When detected directly, it is possible to isolate the virus from the blisters. In the event of an indirect VZV infection, it is necessary to prove a significant increase in the titter of antibodies against the VZV. In shingles, the antibodies are present at the beginning of the disease and the titters rise rapidly and reach higher values. It is not important to examine specific antibodies because anamnestic antibodies are present after suffering from varicella and the antibody response is unreliable. An increase in the titter of antibodies present against the VZV may also occur during the infection of the HSV virus. (3)

Differential Diagnosis

Diagnosing shingles is not difficult given a typical eruption. Prior to the onset of a rash on the chest or back, the pain can mimic the vertebrogenic algic syndrome, radiculopathy or the already-mentioned myocardial attack. There may be a suspicion of otitis of another aetiology if the rash appears around the ear canal. The aetiology must be considered especially in the case of herpes zoster sine herpete and serous meningoencephalitis. Skin changes on a smaller scale may be mistaken for sores caused by herpes simplex. (5) Phytophotodermatitis may even sometimes imitate shingles when accompanied by a blistering rash (Fig.7).


In local therapy, during the acute, wet phase, we apply drying capabilities in galenic forms, which contain a water component (we follow the well-known dermatological rule: wet on wet). Therefore, galenic forms of sprays and pastes are most suitable for ambulatory therapy. The recommended active substances are 10% zinc concentration (ex. Cutozinc 10% spray), 2–3% ichthammol (ex. Cutozinc Ichtamo spray), 1–3% tetracycline and silver (ex. Silvertan® pasta). For hospitalized patients, the medical staff may apply dry compresses (ex. Jarisch solution, 3% boric water). (2,4) Local anti-viral medication is only of limited significance, just like when treating herpes labialis and genitalis. (2,4) Prior to another application, dermatologists recommend using an antiseptic sodium laureth sulphate free syndetic (ex. Cutosan® wash gel) to wash the deposits off. This mechanically removes older external layers, which prevent unwanted occlusions and also directly disinfects the affected surface of the skin. Both mechanisms work synergically against impetiginisation, a frequent complication when healing shingles. Anti-viral medication is the most effective in overall therapy. System-wide therapy using anti-viral medication alleviates the course of the disease and reduces the onset and severity of postherpetic neuralgia. Ideally, patients should begin taking the medication within 72 hours of the onset of the disease. However, if new lesions form, anti-viral medication can be taken anytime during the course of the disease. Acyclovir was the first anti-viral medication used to treat HSV and VZV infections.  It also has an intravenous form, which is used in severe cases on hospitalized patients. Chemically, it is an analogue guanosine that acts like a false nucleotide. Phosphorylation turns into the active substance, acyclovir-triphosphate. Both intracellular enzymes and viral thymidine kinase are involved in triple phosphorylation. Acyclovir-triphosphate then blocks the viral DNA polymerase, which leads to terminating the viral replication. It only reaches effective concentrations in infected cells. Therefore, it is not toxic for the organism. Resistance to acyclovir is described particularly in immunosuppressed individuals. In milder forms, Acyclovir is administered orally, 800mg 5 times a day (every 4 hours with an 8-hour break during the night) for 7 days. The package contains 35 800mg tablets and the dose is modified. (9) The dose should not be lower when treating shingles! Acyclovir is administered intravenously in the cases are more severe. Administering acyclovir is also important in immunocompetent individuals. It shortens the healing time of skin lesions and prevents or at least alleviates postherpetic neuralgia. Acyclovir is intended to treat shingles in children under 12 years of age.

Valacyclovir is currently the more recommended, modern anti-viral medication. It is a prodrug of acyclovir. It is derived from acyclovir by binding it to valine. This increases its biological availability and can effectively be administered later than acyclovir. The effective mechanism is the same as in acyclovir. For shingles, it is administered 3×1000mg per day (2-2-2) for 7 days. The package contains 42 500mg tablets and the dose is modified. (10,11) Additional, effective therapy, also used to prevent postherpetic neuralgia, is combined with Vitamin B (Milgamma N capsules). It is a combination of B1 (benfothiamine), B6 (pyridoxine hydrochloride) and vitamin B12 (cyanocobalamin) derivatives, which are important for the metabolism of the nerve cells. For shingles, it is recommended to take these vitamins together with anti-viral (dose: 1-1-1) and prolong the therapy to at least 30 days. Preferably, the therapy includes immunostimulants (inosine pranobex) . When in pain, take analgesics, usually paracetamol, NSA, nimesulide or mild opioids, ex. tramadol. When experiencing severe pain or severe postherpetic neuralgias, strong opioids, tri-cyclical anti-depressants or anti-epileptics are administered. Depending on the location and severity of the impairment, interdisciplinary cooperation is applied, which involves the participation of a dermatologist, an infectious disease specialist, a neurologist, a specialist in pain treatment, an ophthalmologist or an otorhinolaryngologist. (2)


Herpes zoster is a disease that mainly affects the elderly and patients with other associated diseases. Even a normal or typical course may be bothersome or debilitating for the patient, especially when the acute phase is followed by several months of lasting pain – postherpetic neuralgias. Modern vaccines may limit the occurrence of the disease itself, if it develops. Modern vaccines may also alleviate the course and subsequent problems, like postherpetic neuralgia.

MUDr. et MUDr. Pavel Konrád

Dermatology Clinic

Mokropeská 2027, 252 28 Černošice



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