Case study of Zoster without complications

Case study: Zoster without complications

CHIEF COMPLAINT: Painful ulcerative rash for the past couple of days.

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HISTORY OF PRESENT ILLNESS: The patient is an elderly Hispanic female (aged 73 years) who visits complaining of a painful ulcerative rash for the past couple of days. This rash commences on the posterior right back, radiating to the front right side and going along a dermatomal pattern. The patient reports it is highly painful and pruritic; pain worsens when showering or if clothes touch the area. Nothing appears to alleviate it. Patient’s self- rating of her pain is 7/10. She had contracted chicken pox during her childhood.


The patient reports a painful ulcerative rash which first showed up a couple of days ago. Patient symptoms suggest that she has contracted HZ (Herpes Zoster) or shingles. This is a condition that arises due to VZV (varicella zoster virus) reactivation, which happens with VZV immunity decline owing to immunosuppression or aging. HZ may develop among individuals of any age group; however, the most predominantly impacted group is aged persons (Sampathkumar, Drage & Martin, 2009). It normally presents as the following two separate conditions: chickenpox (primary infection) and HZ or zoster (the secondary condition) (Cohen, Salbu, Frank & Israel, 2013). According to the patient, she had contracted chicken pox during her childhood. Shah, Einstein, Sharma, and Singarju (2016) claim that a majority of individuals contract this virus during childhood and suffer from a bout of chickenpox. Ultimately, the individual’s immune system gets rid of it from a majority of areas; however, the virus may be latent or dormant within dorsal root ganglia (which lie next to one’s spinal cord) or the skull’s ganglion semilunar. A repeated shingles attack is seldom reported.

HZ’s clinical features may be categorized as: (1) acute; (2) chronic; and (3) prodromal. At first, patients come down with a fever, unilateral sensitivity and pain along affected sensory nerves, and overall unease. The trunk is typically impacted. Within some days, linear vesicular or papular mucosa/ skin eruption occurs (Neville, Damm Allen & Bouquot, 2009).

Race can play a role in HZ susceptibility. For instance, Black Americans display 25 percent greater likelihood as compared to White Americans to contracting shingles. While HZ isn’t as infectious as primary varicella, individuals having reactivated infection may transfer VAV to non- immune entities. Rate of household transmission has been found to be roughly 15% (Brody & Moyer, 1997).


HZ treatment has the following three key goals: (1) Acute virus treatment, (2) Postherpetic- neuralgia prevention, and (3) treatment of HZ- related acute pain. The above goals can be attained using antiviral agents, adjunctive personalized pain alleviation modalities, and oral corticosteroids. The former have demonstrated their capability of reducing HZ rash duration and magnitude of HZ rash- linked pain. But the above benefits are only witnessed among individuals receiving the medication within three days of rash development. Antiviral agents can prove useful so long as fresh lesions continue to form; however, following lesion crusting, they aren’t as useful. Antiviral agent efficacy in post- herpetic neuralgia prevention is a more contentious subject. A large number of research works deal with the problem, though with variable findings. On the basis of outcomes of several researches, treatment using Zovirax (i.e., acylovir) seems to moderately reduce post- herpetic neuralgia development. Famvir (famciclovir), Valtrex (valacyclovir) and similar antiviral agents seem comparably effective. Oral corticosteroids have also been popularly utilized when treating HZ, despite clinical trials depicting variable outcomes. A combination of acyclovir and prednisone decreases HZ- linked pain. Caladryl and other calamine- containing lotions can be applied to open lesions for alleviating pruritus and pain (Stankus, Dlugopolski & Packer, 2000).






















Brody, M. B., & Moyer, D. (1997). Varicella-zoster virus infection. Postgrad Med, 102(1), 187–94.

Cohen, K., Salbu, R., Frank, J., & Israel, I. (2013). Presentation and management of Herpes Zoster (Shingles) in the geriatric population. P T, 38(4): 217-224.

Neville, B. W., Damm, D. D., Allen, C. M., Bouquot, J. E. (2009).Viral infections. Oral and Maxillofacial Pathology (3rd ed.), 251–2.

Sampathkumar, P., Drage, L. A., & Martin, D. P. (2009). Herpes Zoster (Shingles) and Postherpetic Neuralgia. Mayo Clinic Proc, 84(3), 274-280.

Shah, S., Singaraju, S., Einstein, A., & Sharma, A. (2016). Herpes zoster: A clinicocytopathological insight. J Oral Maxillofac Pathol, 20(3), 547.

Stankus, S., Dlugopolski, M., & Packer, D. (2000). Management of Herpes Zoster (Shingles) and Postherpetic Neuralgia. Am Fam Physician, 61(8), 2437-2444.


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