Saudi Critical Care Journal

: 2020  |  Volume : 4  |  Issue : 4  |  Page : 130--133

Herpes zoster coinfection and the current COVID-19 pandemic

Irfan Altaf 
 Department of Anesthesiology, Critical Care and Pain Medicine, All India Institute of Medical Sciences, New Delhi, India

Correspondence Address:
Irfan Altaf
Vishram Sadan Complex. Dr Irfan Altaf, JPNATC AIIMS, New Delhi-110 029


Clinical presentation of COVID-19 infection can be variable in the current pandemic, even in patients presenting to the clinic with mild history of upper respiratory complaints. Various cutaneous manifestations have been noticed in COVID-19 patients with herpes zoster (HZ) being one among them. HZ is an infection that results when varicella zoster virus reactivates from its latent state in a posterior dorsal root ganglion. Here, we aim to expand our knowledge by reporting three cases of associated zoster infection in COVID-19 patients admitted to our intensive care unit in view of respiratory complaints. All the three patients admitted had revealed lymphocytopenia at the time of HZ diagnosis and were managed conservatively throughout the course. In all the cases, acyclovir/valacyclovir led to the resolution of lesions in 10 days. No postherpetic sequelae were observed. We hereby suggest that the clinical presentation of HZ at the time of current pandemic should be considered as an alarming sign for a latent subclinical SARS-CoV-2 infection and thorough follow-up of such patients should be adopted.

How to cite this article:
Altaf I. Herpes zoster coinfection and the current COVID-19 pandemic.Saudi Crit Care J 2020;4:130-133

How to cite this URL:
Altaf I. Herpes zoster coinfection and the current COVID-19 pandemic. Saudi Crit Care J [serial online] 2020 [cited 2021 Jan 28 ];4:130-133
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The most recently identified member of the zoonotic pathogens of coronaviruses, SARS-CoV-2, started with an outbreak of pneumonia in Wuhan City of China in December 2019.[1] Although closely related to SARS-CoV and Middle East respiratory syndrome coronavirus, with bat as reservoir, SARS-CoV-2 is markedly more infectious with a high potential for human-to-human transmission. The novel virus was officially named SARS-CoV-2, and the disease termed as COVID-19.[2],[3],[4] Although most patients with COVID-19 exhibit mild-to-moderate symptoms, approximately 10%–15% of them progress to severe pneumonia and roughly 5% of the patients develop complications such as acute respiratory distress syndrome, septic shock, and/or multiple organ failure.[5],[6] A relevant history and clinical examination for recognition of asymptomatic carriers can be very helpful in the management of this outbreak.[1] A wide range of skin manifestations in COVID-19 infection have been reported ranging from erythematous rash, erythema multiforme, to urticarial/chickenpox-like lesions.[7] We encountered three cases of clinically diagnosed herpes zoster (HZ) infection admitted to our hospital. All patients showed mild respiratory symptoms related to COVID-19 infection and denied any history of travel or contact with patients with known COVID-19 infection.

 A Case Series

Case 1

A 52-year-old gentleman presented with painful blisters on the right side of his neck and upper chest. The pain was continuous, severe, and burning in nature. He gave a history of pain followed by the development of blister-like lesions. The lesions were initially small and few in number and now with serous discharge. The area surrounding the vesicular eruption was flared and tender to touch [Figure 1]. The patient denied any such history in the past, except the history of hypertension which is controlled with medication. The patient was prescribed oral acyclovir 500 mg 5 times daily for 1 week, oral prednisolone 20 mg thrice a day for 1 week, and calamine lotion for topical application. Two days following the presentation, the patient started with fever, dry cough, sore throat, and dyspnea required intensive care unit (ICU) admission. Computed tomography (CT) thorax was done which revealed basal and peripheral patchy ground-glass infiltration in both lungs consistent with the findings of COVID-19 infection. A nasopharyngeal swab was also taken and revealed a positive for COVID-19.{Figure 1}

Case 2

A 45-year-old male got admitted with a 3-day history of low-grade fever, myalgia, and a painful vesicular rash on the right side of his neck. On examination, a tender vesicular rash with serous discharge was noted on the right side of the neck. He was prescribed valacyclovir 1 g twice daily for 1 week, prednisolone 5 mg twice daily for 5 days, besides calamine lotion for local application. Oral mucosa was free from such findings [Figure 2] and [Figure 3]. No similar history in the past was revealed. During the course, he became dyspneic and got admitted in the ICU. Pulmonologist consultation was sought for his respiratory symptoms. Meanwhile, chest X-ray was done and nasopharyngeal smear was sent for reverse-transcriptase polymerase chain reaction (RT-PCR) and was later on found to be positive for COVID-19 infection.{Figure 2}{Figure 3}

Case 3

A 37-year-old male presented with a 5-day history of dry cough, loss of smell, and headache. The patient came to the hospital for COVID screening and the patient was kept in the isolation ward. On the same day, the patient reported a sudden onset of itching with painful rash on the right lateral wall of the chest [Figure 4]. The rash appeared as small fluid-filled vesicles that had rupture upon scratching, with clear discharges. The spread of the rash was consistent with T8 dermatome and did not extend beyond the midline, therefore supporting the diagnosis of HZ. Vital signs and rest of the physical examination were normal, except the skin manifestations. Next day, the nasopharyngeal swab turned positive for SARS-CoV-2.{Figure 4}

Diagnosis of COVID-19 disease is made on the grounds of clinical signs such as fever, dry cough, malaise, ageusia, and anosmia as well as radiological findings such as chest CT scan for the presence of ground-glass opacity.[3] The clinical scenario differs with most patients receiving only the supportive care, while others require admission to an ICU for mechanical ventilation or hemodynamic monitoring.[6],[7] Incubation period of COVID-19 can range from 10 to 14 days. Besides the history of travel and close contact, diagnosis can be confirmed by the detection of viral RNA through real-time RT-PCR for nasopharyngeal smear or bronchoalveolar fluid.[3] Elderly patients more than 60 years of age, especially male gender, cardiovascular disease, and other patients with debilitating chronic conditions with immunocompromised status are at an increased risk of severe disease and poor outcome.[6] However, little is known regarding the cutaneous manifestations of COVID-19 patients. Recently, different groups have reported patients with features of skin rash after COVID-19, ranging from erythematous rash to chickenpox-like/urticarial eruption.[7] We encountered the HZ activations in three COVID-19 patients admitted in our ICU revealing characteristic features. In all the cases, acyclovir led to the resolution of lesions in around 10 days' time with no postherpetic neuritic sequelae.

HZ is the infection that results when varicella zoster reactivates from its latent state in the dorsal root ganglia following an early episode of chickenpox. The condition manifests in the form of painful, unilateral vesicles, usually multiple and gets ulcerated and follows a typical dermatomal pattern innervated by single dorsal root ganglion. Involvement of three or more dermatomes is known as disseminated zoster and seen in immunocompromised individuals.[7],[8],[9] One possible explanation of the HZ reactivation could be the reduction in absolute lymphocyte count, especially the CD3+ CD8+ lymphocytes due to SARS-CoV-2 infection.[10] Lower percentages of T-cell functional markers have also been observed within the T-cell population as COVID-19 patients showed decreased percentages of CD-107a+, CD8+; interferon gamma+, CD8+; and interleukin-2+ CD8+ T-cells and mean fluorescence intensity of granzyme B+ CD8+ T-cells when compared to normal controls.[11] It is reasonable to hypothesize that, in addition to the activation-induced cell death, SARS-CoV-2 directly infects lymphocytes, particularly the T-cells, and promotes their cell death of causing lymphopenia and eventually leading to impaired antiviral response.[11] Moreover, functional damage of CD4+ T-cells has been postulated, thereby predisposing to higher grades of severity of the disease COVID-19.[11],[12],[13]

In conclusion, we suggest that during the current COVID-19 pandemic, the clinical presentation of HZ infection, in patients having an associated history of mild upper respiratory complaints, should be considered as an alarming signal for a latent or subclinical SARS-CoV-2 infection. A thorough follow-up of such patients should be adopted and it is prudent to adhere to maximum precautions until the diagnosis of COVID-19 is excluded.

Since the decision to pharmacologically immunosuppress a critically unwell patient with COVID-19 remains a challenge. We therefore suggest, that further studies are needed before the use of immunosuppressive medication, as the possible beneficial effects of reducing the inflammatory response by these agents should be carefully weighed against the delay in viral clearance.[13],[14],[15]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


1Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA 2020;323:1061-9.
2Li Q, Guan X, Wu P, Wang X, Zhou L, Tong Y, et al. Early transmission dynamics in Wuhan, China, of novel corona virus-infected pneumonia. N Engl J Med 2020;382:1199-207.
3Wiersinga WJ, Rhodes A, Cheng AC, Peacock SJ, Prescott HC. Pathophysiology, transmission, diagnosis, and treatment of coronavirus disease 2019 (COVID-19): A Review. JAMA 2020;324:782-93.
4Zhang YZ, Holmes EC. A genomic perspective on the origin and emergence of SARS-coV-2. Cell 2020;181:223-7.
5Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020;395:497-506.
6Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med 2020;46:846-84.
7Wollina U, Karadag AS, Rowland-Payne C, Chiriac A, Lotti T. Cutaneous signs in COVID-19 patients: A review. Dermatol Ther 2020;33:e13549.
8Ahouach B, Harant S, Ullmer A, Martres P, Bégon E, Blum L, et al. Cutaneous lesions in a patient with COVID-19: Are they related? Br J Dermatol 2020;183:e31.
9Dayan RR, Peleg R. Herpes zoster-typical and atypical presentations. Postgrad Med 2017;129:567-71.
10Wang F, Nie J, Wang H, Zhao Q, Xiong Y, Deng L, et al. Characteristics of peripheral lymphocyte subset alteration in COVID-19 pneumonia. J Infect Dis 2020;221:1762-9.
11Henry BM, de Oliveira MH, Benoit S, Plebani M, Lippi G. Hematologic, biochemical and immune biomarker abnormalities associated with severe illness and mortality in coronavirus disease 2019 (COVID-19): A meta-analysis. Clin Chem Lab Med 2020;58:1021-8.
12Wei L, Zhao J, Wu W, Zhang Y, Fu X, Chen L, et al. Decreased absolute number of CD3+ T-cells and CD8+ T-cells during aging in herpes zoster patients. Sci Rep 2017;7:15039.
13Zheng M, Gao Y, Wang G, Song G, Liu S, Sun D, et al. Functional exhaustion of antiviral lymphocytes in COVID-19 patients. Cell Mol Immunol 2020;17:533-5.
14Cao X. COVID-19: Immunopathology and its implications for therapy. Nat Rev Immunol 2020;20:269-70.
15Ritchie AI, Singanayagam A. Immunosuppression for hyperinflammation in COVID-19: A double-edged sword? Lancet 2020;395:1111.