|Year : 2016 | Volume
| Issue : 1 | Page : 21-23
Herpes virus induced bullous lesions in a child with acute leukemia
Amitabh Singh, Anirban Mandal, Rachna Seth
Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India
|Date of Web Publication||4-Jan-2016|
Department of Pediatrics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110 029
Source of Support: None, Conflict of Interest: None
Immunodeficient children are at a risk for development of atypical or extended infection with viral agents, including herpes virus (herpes simplex and herpes zoster). We report a 5-year-old child with B lineage acute lymphoblastic leukemia on chemotherapy with herpes virus induced atypical skin manifestations. Diagnostic possibilities of early toxic epidermo-necrolysis, staphylococcal scalded skin syndrome, pemphigus vulgaris, bullous pemphigoid, and bullous herpetic infection were kept and management with antibiotics, anti-viral, and supportive measures were ensued. Tzanck smear was negative, but skin swab grew methicillin sensitive Staphylococcus aureus. Herpes viral etiology could be established only after the skin biopsy and histopathological examination showed multinucleated cells with intranuclear inclusion body. There was no other systemic involvement except the asymptomatic elevation of transaminases. She was recovered completely with acyclovir therapy for 14 days. Our case highlights the need for heightened awareness among the clinicians for such atypical presentation of common infections in immunodeficient children, as early and prompt institution of therapy can be lifesaving. Though Tzanck smear is a good modality for the diagnosis of herpetic lesions, it should be supplemented with other diagnostic tests and should not be relied upon in isolation to refute the diagnosis.
Keywords: Acute leukemia, herpes virus, immunocompromised host, vesico-bullous lesion
|How to cite this article:|
Singh A, Mandal A, Seth R. Herpes virus induced bullous lesions in a child with acute leukemia. Indian J Paediatr Dermatol 2016;17:21-3
|How to cite this URL:|
Singh A, Mandal A, Seth R. Herpes virus induced bullous lesions in a child with acute leukemia. Indian J Paediatr Dermatol [serial online] 2016 [cited 2020 Jul 7];17:21-3. Available from: http://www.ijpd.in/text.asp?2016/17/1/21/173157
| Introduction|| |
Acute leukemia is the most common malignancy of childhood. Leukemia itself and the chemotherapy used, leads to immunosuppression, predisposing children to various infections caused by bacterial, viral, and fungal agents. Viral infections are particularly common in childhood and in the background of suppressed immunity, both the frequency and severity of such infections increases by manifold. Herpes viral infections are seen universally. Herpes simplex viruses (HSV 1 and HSV 2) are known to cause primary infection during childhood with exacerbations occurring throughout life. Herpes simplex usually presents with single or grouped vesicles over muco-cutaneous junction in oral (HSV 1) or genital regions (HSV 2). Similarly, Herpes zoster virus primary infection leads to varicella or chicken pox presenting with successive crops of diffuse, pruritic vesicles on an erythematous base, evolving into pustules, and ultimately healing with crusting. Reactivation leads to herpes zoster characterized by vesico-pustular lesions on an erythematous background with a distinct dermatomal distribution. Both diagnosis and management of vesico-bullous lesions in children pose a considerable challenge to the pediatrician and dermatologist as the differential diagnosis contains a myriad of diseases ranging from benign conditions to life-threatening systemic problems. We report a pediatric patient with B-lineage acute lymphoblastic leukemia on the maintenance phase of chemotherapy presenting with widespread vesico-bullous eruptions following fever and was later diagnosed to be secondary to the herpes virus.
| Case Report|| |
A 5-year-old girl was diagnosed with B-cell acute lymphoblastic leukemia 2 years back and was on treatment with standard chemotherapy protocol, since then. She was currently on the fifth cycle of maintenance chemotherapy, receiving oral methotrexate weekly, and oral 6-mercaptopurine daily, and was apparently asymptomatic till the present illness. She presented with the complaints of fever for 7 days and vesico-bullous lesion over the body for 3 days. The lesions started as small vesicles over the abdomen and rapidly spread over the whole body with blister formation. There was no preceding history of pain or redness of the skin. On examination, there were vesico-bullous lesions spread all over the body, including palms and soles with surrounding erythema and multiple flaccid blisters with some of the lesions containing purulent material. There was no involvement of mucosal surfaces (e.g., oral, conjunctival, vaginal, or anal). Clinical level of separation appeared to be subcorneal and Nikolsky's phenomenon was absent [Figure 1]. Child's vital parameters and systemic examination were within normal limits. Dermatological consultation was sought and possibilities of early toxic epidermo-necrolysis, staphylococcal scalded skin syndrome, pemphigus vulgaris, bullous pemphigoid, and bullous herpetic infection were kept. Investigations revealed leukopenia (total leucocyte count - 1800/mm 3 and absolute neutrophil count - 1.4 × 103/mm 3) and raised liver enzymes (serum glutamic oxaloacetic transaminase - 204 U/L, serum glutamic pyruvic transaminase - 147 U/L). Tzanck smear from the vesicular lesions did not show any giant cells. She was started on intravenous (IV) antibiotics covering staphylococcus, IV acyclovir, IV fluids, and supportive measures. Hydration and electrolyte balance were taken care akin to the management of burns. Nutrition was managed with nasogastric feeding and management of skin lesions were done with dressing of saline soaked gauze placed over the soft silicone primary dressing of denuded skin. Anti-bacterial (Mupirocin) ointment was applied over the areas of skin having pus discharge. Prevention of hypothermia and early institution of physiotherapy were also initiated help in preventing further morbidity. Blood culture failed to grow any organisms, but skin swab showed abundant growth of methicillin sensitive Staphylococcus aureus. Skin biopsy revealed dermo-epidermal blister formation with blister cavity filled with fibrin and few polymorphs. Few acantholytic cells showed multinucleation, ground glass chromatin, and intranuclear viral inclusions. The detached epidermal cells had necrosis. Features were suggestive of herpes virus induced bullous lesions. Immunohistochemistry or polymerase chain reaction (PCR) for herpes virus could not be done in the specimen to identify the offending virus type in view of nonavailability of such facilities. As there was no previous history of chicken pox in the child, a diagnosis of herpes virus induced bullous lesion with secondary staphylococcal skin infection was made and she was given acyclovir for a total of 14 days with systemic antibiotics. Her skin lesions subsided over next 10 days and currently she is totally asymptomatic with only few scarring over the previous skin lesions.
|Figure 1: Vesico-bullous lesions with multiple flaccid blisters and purulent discharge without any mucosal involvement|
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| Discussion|| |
Viral causes of vesico-bullous lesions most commonly include HSV and varicella zoster virus. Incidence of infection with herpes simplex and herpes zoster virus is increased greatly in immunocompromised hosts., Immunocompromised patients are also at a risk of development of disseminated/extended infection with herpes group of viruses (herpes simplex and herpes zoster).,, Atypical features of skin involvement in the immunocompromised patients include atypical locations, hemorrhagic lesion and larger size of lesions, deeper ulceration, satellite lesions, and longer healing time. The ulcerative-necrotic-gangrenous variety of zoster lesions are exclusively described in the immunocompromised patients. The pathogenesis of such bullous lesions remains unclear and also been implicated to coinfecting exfoliative cytotoxin producing Staphylococcus. The most common secondary bacterial skin infection in varicella is by S. aureus and Streptococcus pyogenes. We could identify methicillin sensitive S. aureus in our patient. Atypical herpes infections in the immunocompromised patients are known to resemble blistering disorders such as bullous pemphigoid, pemphigus vulgaris, or pemphigus foliaceus, posing great difficulty in the diagnosis and management. In the typical cases of herpes viral infection, the diagnosis is mostly clinical, but in the cases of atypical presentation, Tzanck smear, tissue biopsy, viral culture, electron microscopy, and PCR to detect herpes virus DNA can be utilized to establish the diagnosis. The Tzanck smear is an easy, fast, and inexpensive test with a reported sensitivity rates ranging from 73% to 100%. However, its sensitivity also depends upon the observers' experience, the type, and duration of the lesions. Ideally, the smear should be prepared from intact, fresh (1–3 days) blisters after deroofing and if blisters are absent, wet or eroded lesions are preferred over crusted lesions. High morbidity and mortality rates are described in the immunocompromised patients with herpes virus infection,, but fortunately our patient only had asymptomatic elevation of transaminases. She could be treated successfully upon the early institution of acyclovir therapy, continued for 14 days as per the recommendations.
| Conclusion|| |
Our case emphasizes on the importance of clinical awareness of extended and atypical clinical presentations of herpes viral infections in the immunocompromised patients and also that timely diagnosis and appropriate management will improve the outcome. Negative Tzanck smear should not be relied upon solely to exclude the diagnosis and other diagnostic approaches are to be applied, especially when the clinical suspicion is high.
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.
| References|| |
Sanfilippo AM, Barrio V, Kulp-Shorten C, Callen JP. Common pediatric and adolescent skin conditions. J Pediatr Adolesc Gynecol 2003;16:269-83.
Eichenfield LF, Honig PJ. Blistering disorders in childhood. Pediatr Clin North Am 1991;38:959-76.
Veraldi S, Carrera C, Gianotti R, Caputo R. Bullous herpes zoster. Acta Derm Venereol 2000;80:55.
Wong KJ, Osowicki J, Seaby E, Curtis N, Gwee A. Bullous herpes zoster. J Pediatr 2014;164:667.
Burgoyne M, Burke W. Atypical herpes simplex infection in patients with acute myelogenous leukemia recovering from chemotherapy. J Am Acad Dermatol 1989;20:1125-6.
Aebi C, Ahmed A, Ramilo O. Bacterial complications of primary varicella in children. Clin Infect Dis 1996;23:698-705.
Madkan V, Sra K, Brantley J, Carrasco D, Mendoza N, Tyring SK. Human herpes viruses. In: Bolognia JL, Jorizzo JL, Rapini RP, editors. Dermatology. 2nd
ed. Philadelphia: Elsevier; 2008. p. 1199-204.
Ozcan A, Senol M, Saglam H, Seyhan M, Durmaz R, Aktas E, et al.
Comparison of the Tzanck test and polymerase chain reaction in the diagnosis of cutaneous herpes simplex and varicella zoster virus infections. Int J Dermatol 2007;46:1177-9.
Gnann JW Jr. Varicella-zoster virus: Atypical presentations and unusual complications. J Infect Dis 2002;186:S91-8.
Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M, et al.
Recommendations for the management of herpes zoster. Clin Infect Dis 2007;44:S1-26.