Rev Chil Infect 2009; 26 (4): 356-359 CLINICAL CASE herpetic eczema herpes simplex virus type 2. Review of the literature apropos of a case Eczema Caused by herpes simplex herpeticum virus type 2. Review of the literature About one case Francisca H. Schroeder, Andrea Elgueta N. and M. José Martínez G. Barros Luco-Trudeau Hospital, Santiago, Chile Service of Dermatology and Venereology (FSH, AEN) University of Chile, Santiago School of Medicine ICBM-Virology Program (MJMG) Correspondence to:
Eczema is an EXTENSIVE herpeticum vesicular eruption Caused by cutaneous dissemination of herpes simplex virus in Patients Who Have underlying skin conditions or epidermal barrier disruption. Herpes simplex virus type 1 (HSV 1) The most common etiology is. This is the first report in Chile of a case of eczema herpeticum Caused by HSV 2 in a patient With Darier ‘s disease, We review the literature and Emphasize the use of sensitive and specific Assays Real as time Polymerase Chain Reaction, That allow to initiate Timely the correct treatment. Key words: Eczema herpeticum, Kaposi varicelliform eruption, herpes simplex virus type 2. Summary Herpetic vesicular rash Eczema is a skin caused by extensive spread of herpes simplex virus in patients with previous skin disorders or damage to the epidermal barrier. The most common cause is herpes simplex virus type 1 (HSV 1), although there have been cases of herpes simplex virus type 2 (HSV 2). We present the first report in Chile eczema herpetic HSV 2 in a patient with Darier disease. We review the literature and emphasize the importance of using sensitive and specific as the polymerase chain reaction (RPC) in real time, which allow early initiation of appropriate therapeutic techniques. Keywords: Herpetic eczema, rash varicelliform sarcoma, herpes simplex virus type 2. Introduction Eczema is herpetic cutaneous dissemination of herpes simplex virus in patients with chronic skin diseases, especially atopic dermatitis. It also occurs in patients with other chronic skin diseases (Darier’s disease, pityriasis rubra pilaris, psoriasis and other less frequent), or who have damage to the epidermal barrier.
Most of the cases described in the literature are caused by HSV 1 2-6 and there are only a few reported cases of eczema herpetic HSV 27,8. We present the first report of herpetic eczema HSV 2 in our country. Clinical case 45 year old man, previously healthy, derived from the ES to the Dermatology Department of Hospital Barros Luco Trudeau, by a picture of two weeks of evolution, characterized by acute and progressive appearance of skin lesions on the trunk. In the clinical history only he highlighted the history of a recurrent eruption of the trunk from 18 years of age, characterized by asymptomatic erythematous papules in the sternum region and arms. No history of herpes infections of the skin or genitals, skin diseases or family. Physical examination was in good general, afebrile condition and had multiple papules and pustules on the trunk umbilication, confluent, with some lesions scab stage (Figures 1 and 2). No injuries to the face, genitals and mucous membranes. In the hands he revealed the presence of skin-colored papules flattened on the back, palmar pits and alternating red and white lines on the nails, findings suggestive of Darier disease (Figure 3). He was hospitalized with a presumptive diagnosis of herpetic eczema and Darier’s disease. general examinations, current culture and polymerase chain reaction (RPC) for herpes simplex virus pustules, and biopsy of skin lesions suggestive of Darier’s disease were performed. Empirically treatment with oral acyclovir indicated 400 mg 5 times a day and ev cloxacillin 1 g every 6 hrs, which was maintained for 10 days. Among the general tests normal blood count, VHS 29 mm / h, CRP 123 mg / L, GGT 108 U / L was found.
The results of the VDRL and serology for HIV and HBV were negative. The skin culture was positive for methicillin-resistant Staphylococcus aureus only clindamycin and erythromycin, and real-time PCR, conducted at the Laboratory of Virology of the Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, was positive for HSV 2 . histopathologic findings of skin biopsy were consistent with Darier disease. The patient responded quickly to treatment, he was discharged after 10 days. Discussion Patients with chronic skin diseases, especially atopic dermatitis carriers are at increased risk of developing a skin spread of certain viruses such as herpes simplex virus, Coxsackie virus and the virus Alo vaccinia1,9,10. This clinical picture is known as Kaposi chicken pox rash. The most common cause of Kaposi varicelliform eruption, is the spread of herpes simplex virus in atopic patients, which has been called more specifically herpetic eczema. However, the term herpetic eczema also used for cutaneous dissemination of herpes simplex virus in patients with other chronic skin diseases (Darier’s disease, cutaneous T-cell lymphoma, pityriasis rubra pilaris, benign familial pemphigus, erythroderma congenital ichthyosiform dermatitis seborrheic, Wiskott-Aldrich syndrome, psoriasis, lupus erythematosus) or having epidermal barrier damage (contact dermatitis, burns, grafts, dermabrasion). Similarly, the spread of vaccinia virus in atopic patients (or carriers of other dermatoses) vaccinatum1 known as eczema. Currently, vaccination against smallpox (eradicated disease in the world at the end of the 1970s) is indicated only in emergency situations (Outbreak) and laboratory personnel or health workers who are at risk of acquiring the vaccinia virus or related viruses. Because eczema vaccinatum is a serious complication of this vaccine, the CDC of Atlanta believes that the personal history of atopic dermatitis is a contraindication to vacunación1,11,12. Have been proposed various immuno-logical mechanisms to explain eczema herpeticum in atopic patients: impaired immunity against herpes simplex virus mediated by T cells, a defect in the specific antibodies to the virus, a decrease in NK cells and receptors IL-2, an inhibition of Th-1 response by increased IL-4, decreased cathelicidins (a family of antimicrobial peptides that are part of the innate immunity) or a decrease in producing plasmacytoid dendritic cells interferon I1,13 type.
Another possibility is simply viral spread is facilitated by the disruption of the skin barrier that exists in both atopic dermatitis and other skin conditions associated with eczema herpético1. A retrospective clinical study of 100 cases of herpetic eczema showed as only risk factors, early age of onset of atopic dermatitis and high total IgE levels in atopic and ruled out the use of topical corti-costeroides as predisponente14 factor. Some case reports and prospective studies have found an association between the use of topical calcineurin inhibitors in atopic patients and the development of eczema herpético15-19. Herpetic eczema may result from a primary infection or a recurrence of herpes simplex virus. Most reported cases have been caused by HSV 1 2-6 and only found two cases published by 27,8 VHS. Coincidentally both cases HSV 2 occurred in patients with Darier’s disease, a rare disorder of keratinization, autosomal dominant inheritance with variable penetrance, characterized by hyperkeratotic papules in seborrheic areas, manifested at puberty, with exacerbations and remissions along the life3. The primary form of herpetic eczema (or first episode) is characterized by a monomorphic rash consisting of vesicles that progress to vesicular-pustules umbilication and may coalesce forming crusted plates with varying degrees of bleeding, disease characteristics. Lesions first appear on the skin damaged by the underlying pathology and gradually spread in 7 to 10 days, accompanied by fever, chills skin and lymph nodes. There are also localized forms, without extensive dissemination. The average disease duration is 16 days (range 2 to 6 weeks) 1. 13. Between 13 and 16% of patients may develop recurrent episodes of eczema herpético14. In these cases, the clinical picture is more limited, less commitment general1,13 state.
The most common complication of these patients is bacterial-infection of the lesions, S. aureus being isolated more frecuencia20 agent. More serious complications are secondary viremia with involvement of other organs, bacterial sepsis or ocular herpes simplex virus infection. Despite the high frequency of facial injuries, herpetic keratitis is rare, even in patients who have isolated virus conjuntival1,13 mucosa. The clinical diagnosis of eczema herpeticum should be suspected in the presence of distinctive lesions in a patient with impaired skin barrier base, especially atopic dermatitis. The main differential diagnoses are VZV infection, impetigo and contact dermatitis. The presence and type of herpes simplex virus involved may be confirmed by viral, immunofluorescence or RPC torula a specimen obtained vesicle floor insulation. If this is not possible, the presence of giant cells in the test Tzanck can guide the diagnosis of herpes infection; its sensitivity can reach 70% depending on the state of the injury, it is a rapid, inexpensive method which allows early initiation of antiviral treatment. Skin biopsy shows characteristic histological changes of herpetic infection (epidermis with intra- and intercellular edema, intranuclear inclusion bodies eosinofilíeos and multinucleated giant cells). If a bacterial super-infection of lesions suspect a corriente1,13 culture should be performed. The mainstay of treatment of herpetic eczema is active nucleoside analogues against herpes simplex virus, such as acyclovir or valaciclovir, which has decreased the lethality of this disease from 50% to less than 10% 13. There is a controlled, multicenter, double-blind, randomized clinical trial comparing 200 mg 5 times daily oral acyclovir for 5 days versus placebo in 60 immunocompetent patients. This study showed that acyclovir therapy in these doses accelerates clinical recovery of patients and reduces the duration of ulcers, with all patients without lesions on the tenth day of starting treatment.
a significant difference in duration of viral excretion groups8 between the two was not found. However, since the herpetic eczema is a serious pathology is recommended valacyclovir (1 g every 8 hours for 7 to 10 days, depending on patient outcomes), due to their greater biodisponibilidad1. It should be noted also that acyclovir could be used ev, according to the severity of the patient. References 1. Kramer S, Tilomas C, Tyler W, Elston D. Kaposi’s varicelliform eruption: A case report and review of the literature. Cutis 2004; 73: 115-22. [Links] 2. Pantazi V, Potouridou I, Katsarou A. Papadogiorgaki H, Katsambas A. Darier’s disease complicated by Kaposi’s varicelliform eruption due to herpes simplex virus.
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Arch Dermatol 1977; 113: 1085-6. [Links] 8. Niimura M, Nishikawa T. Treatment of eczema herpeticum With oral acyclovir. Am J Med 1988; 85 (2A): 49-52. [Links] 9. Monckton Copeman P-W, H Wallace J. Eczema vaccinatum. Br Med J 1964; 2: 906-8. [Links] 10.
Salo O P, M J. Valle Eczema vaccinatum in a family with Darier’s disease. Br J Dermatol 1973; 89: 417-22. [Links] 11. Engler R J, Kenner J, Leung D Y. Smallpox vaccination: Risk considerations for Patients With atopic dermatitis. J Clin Immunol 2002 Allergy; 110: 357-65. [Links] 12. Cono J, Casey C G, Bell D M; Centers for Disease Control and Prevention. Smallpox vaccination and adverse reactions. Guidance for Clinicians.
MMWR Recomm Rep 2003; 52 (RR-4): 1-28. [Links] 13. K. McKenna J Kaposi varicelliform eruption. www. emedicine. com/derm/topic204. htm (accessed 17 September 2008). [Links] 14. Wollenberg A, Zoch C, Wetzel S, G Przybilla Plewig B. Predisposing factors and clinical features of eczema herpeticum: a retrospective analysis of 100 cases.
J Am Acad Dermatol 2003; 49: 198-205. [Links] 15. – Lübbe J, Pournaras C C, J H. Saurat herpeticum Eczema atopic dermatitis During treatment of 0. 1% tacrolimus ointment With. Dermatology 2000; 201: 249-51. [Links] 16. Miyake M-Kashima, K. Tanaka M Fukagawa, Takano Y, Dogru M, Asano-Kato N. et al. Kaposi varicelliform 0.
1% eruption Associated With tacrolimus ointment in atopic blepharitis treatment. Cornea 2004; 23: 190-3. [Links] 17. Papp K A, Werfel T, Fölster-Holst R; Ortonne J P, P C Potter, Prost Y, et al. Long-term monitoring of atopic dermatitis pimecrolimus cream 1% With infants and young children in: a two-year study. J Am Acad Dermatol 2005; 52: 240-6. [Links] 18. – Paul C, M Cork, Rossi A B, Papp K A, Barbier N, Y. Prost Safety and tolerability of 1% pimecrolimus cream Among infants: Experience with 1,133 Patients Treated for up to 2 years. Pediatrics 2006; 117: ell8-28. Epub 2005 Dec 15.
[Links] 19. Osawa K, Etoh T, Ariyoshi N, Ishii I, Ohtani M; Kariya S, et al. Relationship Between Kaposi’s varicelliform eruption in Japanese Patients With atopic dermatitis Treated With tacrolimus ointment and genetic polymorphisms in the IL-18 gene promoter region. J Dermatol 2007; 34: 531-6. [Links] 20. – Brook I, Frazier E H, J Yeager K. Microbiology of infected eczema herpeticum. J Am Acad Dermatol 1998; 38: 627-9. Rev Chil Infect 2009; 26 (4): 356-359 [Links] Received: March 28, 2008 Accepted: January 20, 2009 Correspondence to:
Francisca Schroder Hanke lulateno@hotmail. com