INTRODUCTION

Herpes zoster (HZ) is viral infection because the reactivated of the Varicella

zoster virus (VZV), the same virus who responsible for chickenpox. HZ is more

commonly known as shingles, from the Latin cingulum, for “girdle”. This is

because a common presentation of HZ involves a unilateral rash that can wrap

around the waist or torso like a girdle.1,2

Herpes zoster occurs only occasionally before the age of 50, and at least half

of more than 1 million cases in the U.S. annually occur among people older than

age 60.3 There is no way to predict who will develop HZ, when the latent virus

may reactivate, or what may trigger its reactivation. However, the elderly and

those with compromised immunity–such as those who have undergone organ

transplantation or recent chemotherapy for cancer, or individuals with HIV/AIDS

–are at greater risk for developing HZ. Between 10-20 percent of normal

(immunocompetent) adults will get shingles during their lifetime.1

VZV is one of eight known herpes viruses that infect humans. Primary

infection is clinically identified as Varicella or chickenpox. VZV is ubiquitous

and highly contagious, with initial exposure typically occurring during childhood.

The virus enters the host via the respiratory system, replicates at an undefined site

(presumably the nasopharynx), infiltrates the reticuloendothelial system, and

eventually makes its way into the bloodstream. Evidence of viremia is manifested

by the scattered nature of the telltale skin lesions on the body.1

Once the initial outbreak has subsided, VZV then retreats into the dorsal

root ganglia, usually sensory, or cranial nerve ganglia where it can lie dormant for

years until some excitatory factor triggers the reactivation. The associated

outbreak is then clinically identified as HZ or shingles. The dermatomal

distribution of the subsequent vesicular rash corresponds to the sensory fields of

infected neurons within a ganglion.1,3

The classic presentation of HZ starts with a prodrome of mild-to-moderate

burning or tingling (or in some cases numbness) in or under the skin of a given

dermatome, often accompanied by fever, chills, headache, stomach upset, and

general malaise. Within 48-72 hours from the prodrome, an erythematous,

maculopapular rash forms unilaterally along the dermatomeand rapidly develops

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into vesicular lesions reminiscent of the original chickenpox outbreak.1 Abnormal

sensation or pain, often described as burning, throbbing or stabbing, occurs in

approximately 75% of patients and may be the first noticeable feature. Often

pruritus in the affected region is the most prominent feature.2 The lesions usually

begin to dry and scab 3-5 days after appearing. Total duration of the disease is

generally between7-10 days. However, it may take several weeks for the skin to

return to normal.1

An appropriate diagnosis of HZ is aided by the appearance of a vesicular

rash with characteristic distribution. When the presentation of skin lesions is not

as clear, as may be the case with immunocompromised patients, laboratory

confirmation is recommended. The polymerase chain reaction (PCR) technique is

the most sensitive and specific diagnostic test, as it can detect VZV DNA in fluid

from the vesicle. Viral culture is possible but typically has low sensitivity. Use of

direct immunofluorescence assay is a good alternative to PCR. It is preferred over

viral culture, as it is more sensitive, of lower cost, and offers a more rapid

turnaround time.1

Treatment for herpes zoster consists of both drug therapy (conventional

therapy) and non-drug (natural therapy).3 The objective of conventional therapy in

the treatment of HZ is to accelerate healing of the lesions, reduce the

accompanying pain, and prevent complications. Medications typically prescribed

include antiviral agents, corticosteroids, analgesics, non-steroidalanti-

inflammatory drugs (NSAIDS), and tricyclic antidepressants.1

As with conventional protocols, the objective of natural therapeutics in the

prevention and treatment of HZ is to facilitate healing of skin lesions, reduce pain,

and prevent complications. Natural therapies can provide solutions to effectively

manage herpes viruses, prevent and treat complications, and minimize the risk of

developing viral resistance. Maintaining adequate nutrition is one contributing

factor to ensuring healthy cell-mediated immunity. 1

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CASE REPORT

Identity of patient

Name : IJ

Sex : Male

Registration number : 0-89-89-77

Age : 53 years old

Address : Ketapang

Phone number : 08126939796

Examination Date : December 6th 2012

History

The Chief Complaint :

Vesicles on the left side of the thorax since 1 week before admission.

History of Present Illness:

Patient came to the hospital complained vesicles develops upon the

erythematous base without any pain, itchy and burning sensation on the left

side of the thorax since 1 week before admission. At first, patient found

reddish rash around his left thorax which becoming vesicle that slightly

spread around his left back. Patient also felt his body becomes weak and

convinced of fever for a few days. At hospital, fever was not found

anymore. Patient denied he got any headache or photophobia.

History of Previous Illness:

Patient never complained like this before. He ever got varicella when he was

young.

History of Family Disease:

None of his family had this kind of disease.

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History of Treatment :

Patient had done chemotheraphy for final cycle due to lung neoplasm stage

IV 2 months ago.

History of Social Habits:

Patient take a bath twice daily with good sanitary. Patient was a non-

alcoholic, and already stop smoking for years.

Physical Examination

Vital Sign:

Not checked.

Dermatological status :

a/r thoraxalis sinistra anterior et posterior found group vesicles and bullous

on an erythematous base with some lesion already crusted, zosteriform

arrangement, some lesion are confluens and there is normal skin among the

lesion, lentikuler in size, and unilateral distribution along the left T4-T7

dermatomes.

Clinical Test

No clinical test available.

Differential Diagnosis

1. Herpes Zoster at regio thoracalis sinistra along the left T4-T7

dermatomes

2. Bullous Impetigo

3. Dermatitis Herpetiformis

Planning Diagnosis

Tzank smear, but not checked. If this tzank test being checked to people

with VZV, as result a multinucleated giant cell will be found in microscopic

examination.

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Diagnosis

Herpes Zoster at regio thoracalis sinistra along the left T4-T7 dermatomes

Treatment

Systemic Medication:

Antiviral: Acyclovir 5 x 800 mg (for 7 days)

Vitamin B Compleks 3x1 tablet

Topical Medication:

- Apply compresses normal saline for the wet lesions or Salicylicum

Acidum 2% for dry lesions

- If the lesions get erosion, apply sodium fusidate over the lesion.

Education

1. Do not touch or scratch and contaminate the lesions.

2. Keep the cutaneous lesions clean (soap and water) and dry to prevent

secondary infections.

3. Wear loose-fitting clothing for improved comfort.

4. Rest well and eating foods with high calorie/high protein.

5. Avoid contact with susceptible infants or small children, susceptible

pregnant women or potentially susceptible immunocompromised

individuals.

Prognosis

Quo ad Vitam :Dubia ad bonam

Quo Ad Functionam :Dubia ad bonam

Quo ad Sanactionam :Dubia ad bonam

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First visit at December 6th, 2012

Dermatologic Status :

a/r thoracalis sinistra anterior et posterior found group vesicles and bullous on

an erythematous base with some lesion already crusted, zosteriform

arrangement, some lesion are confluens and there is normal skin among the

lesion, lentikuler in size, and unilateral distribution along the left T4-T7

dermatomes

Figure 1. First visit at December 6th, 2012. Group vesicles and bullous on an erythematous base with some lesion already crusted along the left T4-T7 dermatomes. A. Left side of thorax B. Left back.

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A B

DISCUSSION

Herpes zoster remains an important medical problem throughout the world

which can occur in anyone who has had varicella.4-6 Herpes zoster, or shingles, is a

localized disease characterized by unilateral radicular pain and a vesicular rash

limited to the area of skin innervated by a single dorsal root or cranial sensory

ganglion.7,8 The characteristic rash and associated pain occur when varicella-zoster

virus, which becomes dormant in sensory ganglia following primary varicella-

zoster virus infection, is reactivated, often in association with declining cellular

immunity associated with advancing age, certain diseases (such as HIV infection),

or effects of immunosuppressive therapy.3-5 Herpes zoster occurs only

occasionally before the age of 50, and at least half of the more than 1 million

cases in the U.S. annually occur among people older than age 60.3

Similarly to this case, a 53-years-old male who had undergone

chemotherapy presented to the hospital with chief complaint of vesicles develops

upon the erythematous base without any pain, itchy and burn sensation on the left

side of the thorax since 1 week before admission. Before the vesicles emerged,

patient found reddish rash around his left thorax which becoming vesicles that

slightly spread around his left back.

Patients with neoplastic diseases (especially lymphoproliferative cancers),

those receiving immunosuppressive drugs (including corticosteroids), and organ-

transplant recipients are at increased risk for shingles.5 Immunosupressed patients

have a 20 to 100 times greater risk of herpes zoster than immunocompetent

individuals of the same age. Immunusuppressive conditions associated with high

risk of herpes zoster include human immunodeficiency virus (HIV) infection,

bone marrow transplant, leukemia and lymphoma, use of cancer chemotherapy,

and use of corticosteroids.8 However, a search for an underlying cancer is not

warranted in otherwise healthy patients in whom herpes zoster develops.5

The triggers for reactivation of VZV have not been identified and probably

involve multiple factors. However, specific components of cell-mediated

immunity (CMI) have an important role in controlling the development of zoster

by preventing reactivation within the neuron or the full clinical expression of

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reactivated VZV as zoster. The effectiveness of these protective components of

CMI is well maintained in immunocompetent persons during childhood and early

adulthood. These CMI components are believed to be partially or substantially

maintained by periodic immunologic boosting. “Endogenous boosting” might

occur in response to subclinical reactivation of latent VZV or to development of

zoster itself, and “exogenous boosting” might occur in response to exposure to

VZV circulating in the population as chickenpox. Although virtually all adults are

infected with VZV, specific immunologic parameters have not been identified to

distinguish who will develop zoster. Although CMI is necessary for the control of

zoster, other nonimmunologic factors also might be involved.7-9

The clinical features of acute zoster is variable.9 Herpes zoster usually

begins with a prodrome, such as pain, itching or tingling in the area that becomes

affected. Typically, patients experience headache, malaise and sometimes

photophobia or fever. Abnormal sensation or pain, often described as burning,

throbbing or stabbing, occurs in approximately 75% of patients and may be the

first noticeable feature. Often pruritus in the affected region is the most prominent

feature.2 Cutaneous involvement may be patchy or confluent, with skin changes

beginning with redness and inflammation followed by the development of clusters

of small or clear vesicles.3

According to the case, patient ever felt his body becoming more weak and

he also got fever for a few day that indicate prodrome state of herpes zoster

clinical features. However, he denied to experienced headache, photophobia and

even pain or itchy. This conditions presumably because of the adverse effect of

chemotherapy. Patient had already done final cycle of chemotherapy for lung

neoplasm stage IV in last two months.

The zoster rash is usually unilateral and does not cross the mid-line,

erupting in one or two adjacent dermatomes. The frequency of zoster occurrence

in different dermatomes has been evaluated in certain studies.9 However, in some

cases, the virus may afflict the cranial nerves, which can lead to complications.1,3

The dermatomes from T3 to L3 are most commonly involved in HZ (Figure 2).

So, the most commonly involved area are thoracic (53%), followed by cervical

(20%), cranial especially trigeminal (15%), and lumbar (11%); sacral dermatomes

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are least frequently involved.3,6 Based on the case, the lesions appear on the left

side of the thorax which refers to T4-T7 dermatomes that compliance as the most

commonly involved dermatomes in HZ.

Figure 2. Dermatomes involved in Herpes Zoster1

The zoster rash itself morphologically evolves from a maculopapular rash to

one comprising clusters of vesicles that ulcerate and crust over the course of 7–10

days. Healing is usually complete by 2–4 weeks. When all lesions have crusted

the rash is considered non-infectious. Residual scarring and pigmentation is

common.2 In immunocompromised patients, zoster initially might present

typically.9,10 However, the rash tends to be more severe and its duration prolonged

on this patient.

9

By its classical manifestation, the signs and symptoms of zoster are usually

distinctive enough to make an accurate clinical diagnosis once the rash has

appeared.9 Thus, patient on this case is diagnosed with Herpes Zoster at regio

thoraxalis sinistra along the left T4-T7 dermatomes.

Although HZ is generally regarded as a self-limited condition, the fact it can

take several weeks to resolve and has the potential for development of

complications such as PHN presents a challenge to clinicians.1

Currently, treatment of HZ with antiviral medication appears to be the

method of choice, particularly when treating elderly and immunocompromised

patients. Although multiple clinical investigations have demonstrated efficacy in

reducing both duration of the rash and severity of the associated pain, benefit has

only been demonstrated in patients who receive treatment within 72 hour/s after

onset of the rash.1 Unless to the patients with zoster ophthalmicus should receive

antiviral therapy even if it is delayed beyond 72 hours. Similarly, consideration

should be given to treating immunocompromised patients or those with

disseminated disease because in immunocompromised individuals who get herpes

zoster may have prolonged viral shedding.2,11 Based on this consideration, the

patient as in this case are still given an antiviral medication, which is oral

Acyclovir five times daily with doses 800 mg for 7 days.

Antiviral drug therapy accelerates the healing of skin lesions and reduces

the duration of pain, presumably by limiting the extent of damage done to the

involved sensory nerves by the replicating of VZV and by shortening the duration

of new lesion formation.3 Three oral antiviral drugs are approved by FDA for

treatment of herpes zoster is acyclovir, valacyclovir and famciclovir. Valacyclovir

and famciclovir are now preferred in practice because they have a simplified

dosing schedule and improved pharmacokinetic characteristics compared with

acyclovir. But in other hand, valacyclovir and famciclovir has been found to be

more cost effective.3

Oral corticosteroids have commonly been used for pain management in

HZ.1 But, in this case, there is no place of using corticosteroids because patient

already in immunocompromised state as a consequence of his chemotherapy for

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lung neoplasm stage IV yet patient also do not complained any pain in the

affected area so far. Thus, analgesics or NSAIDs also have no role in this case.

The objective of natural therapeutics in the prevention and treatment of HZ

is to facilitate healing of skin lesions, reduce pain, and prevent complications. An

underlying goal for employing natural therapies is to strengthen cell-mediated

immunity, thereby allowing the body’s natural defense mechanisms to control the

virus and prevent recurrence. Natural therapies can provide solutions to

effectively manage herpes viruses, prevent and treat complications, and minimize

the risk of developing viral resistance.1

The prognosis of herpes zoster in this case is dubia ad bonam. Most people

recover completely from an acute episode with no pain and skin color returns to

normal. Once you have had shingles, it is unusual for the condition to

return. Shingles comes back in only about 2% of people, but in up to 20% of

people with AIDS. Long-term complications from shingles, such as post-herpetic

neuralgia, may continue for months or many years. The disease also may cause

varying degrees of skin discoloration, primarily darkening.

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DAFTAR PUSTAKA

1. Roxas M. Herpes Zoster And Postherpetic Neuralgia: Diagnosis and Therapeutic Consideration. Alternative Medicine Review Vol. 11, No. 2, 2006: 1-10.

2. Wehrhahn MC, Dwyer DE. Herpes Zoster: Epidemiology, Clinical Features, Treatment And Prevention. Australian Prescriber Vol. 35, No. 5, October 2012: 143-146.

3. Coldwell J, DuBosar R, Alguire P, Bader M. An Internist’s Guide To Preventing, Diagnosing And Treating Herpes Zoster, ACP Observer Extra. American College of Physicians, Independence Mall West, Philadelphia, 2007: 2-7

4. Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Valaciclovir Compared With Acyclovir For Improved Therapy For Herpes Zoster in Immunocompetent Adults. Antimicrobial Agents And Chemotherapy Vol. 39 No. 7, July 1995: 1546-1551.

5. Gnann JW, Whitley RJ. Herpes Zoster. N Engl J Med, Vol. 347, No. 5, August 1, 2012: 340-35.

6. Champion RH, Burton JL, Ebling FJG. Textbook of Dermatology Rook/Wilkinson/Ebling Vol. 2, Fifth Edition. Oxford Blackwell Scientific Publications, 1992: 885-891.

7. Oxman MN. Herpes Zoster Pathogenesis and Cell-Mediated Immunity and Immunosenescence. J Am Osteopath Assoc, Vol.2, No. 6, June 2009: 513-517.

8. Wolff K, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ. Fitzpatrick’s Dermatology In General Medicine, Vol. 2, Seventh Edition. The McGraw-Hill Companies, Inc; 2008: 1885-1898.

9. Harpaz R, Ismael R, Sanchez O, Seward JF. Prevention of Herpes Zoster: Recommendations of The Advisory Committee on Immunization Practices (ACIP). Department of Health And Human Services Centers for Disease Control And Prevention. Morbidity and Mortality Weekly Report Vol. 57, June 6, 2008: 2-13.

10. Division of Epidemiology and Imunization Massachusetts Department of Public Health. Herpes Zoster: Infection Control Guidelines for Long-Term Care Facilities. Massachusetts University; 2007.

11. Immunization Branch California Department of Public Health. Guidelines for The Investigation And Control of Varicella Outbreaks. California, The Institute; February 2007.

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