Disseminated herpes simplex virus in an immunosuppressed patient Mark Haeberle, MD, University of Louisville Division of Dermatology, Louisville, KY, United States; Janine Malone, MD, University of Louisville Division of Dermatology, Louisville, KY, United States; Shannon Mcallister, MD, University of Louisville Division of Dermatology, Louisville, KY, United States
Mucocutaneous manifestations of the Chikungunya virus Jacqueline Guidry, MD, Center for Clinical Studies, Houston, TX, United States; Christopher Downing, MD, Center for Clinical Studies, Houston, TX, United States; Stephen Tyring, MD, PhD, Center for Clinical Studies, Houston, TX, United States
Background: Herpes simplex virus is a DNA virus and is a widespread pathogen. Gingivostomatitis is the most common presentation of primary infection while grouped, painful or pruritic vesicles are most often seen in secondary reactivation. The virus lies dormant in the dorsal root ganglia and reappears in times of decreased immune surveillance. Systemic disease can be seen in some individuals but disseminated cutaneous disease is a rare presentation. Observation: The patient is a woman in her 40s with a 10 day history of a generalized rash. She has a history of acute lymphoblastic leukemia in remission status post allogeneic bone marrow transplant in 2012 and a right eye enucleation due to mucormycosis also in 2012. The patient reported starting a bisphosphonate several weeks prior to presentation. After her first dose, she developed swelling and tenderness involving her left cheek. She was evaluated in the emergency department where a computed tomography scan was performed which returned normal. She was discharged with a suspected cutaneous drug eruption but the following day her rash disseminated and demonstrated vesiculation. Following hospital admission with empiric broad spectrum antibiotic and antifungal therapy, a dermatology consultation was requested. Examination revealed a widespread erythematous, lichenoid eruption with some areas of vesiculation. Oral examination revealed a nontender large ulcer with scalloped borders involving the left soft palate and several coalescing erosions involving the left buccal mucosa. Biopsy of a cutaneous lesion revealed intraepidermal vesicular dermatitis with acantholysis and viral cytopathic effect consistent with herpesvirus infection. Tissue cultures returned positive for herpesvirus infection. Following administration of intravenous acyclovir the patient’s condition improved gradually.
The chikungunya virus has made its endemic debut in the United States. The illness was initially discovered in Africa in 1952 and outbreaks have since been reported in Africa, South Asia, and Southeast Asia. The first case of chikungunya was reported in the United States in 2006, and since over 200 cases have been reported; however, the virus was previously limited to imported cases in which individuals had traveled outside of the United States and returned with the disease. On July 17, 2014, the first chikungunya case acquired in the continental United States was reported by the CDC. The patient was located in Florida, which is not unexpected given that endemic chikungunya has been present in the Caribbean since 2013. The virus is transmitted by the Aedes aegypt and Aedes albopictus mosquito in a pattern similar to that of dengue fever. The virus name is derived from the Makonde language, spoken by an ethnic group of the same name in southeast Tanzania and northern Mozambique. The name is derived from a word that translates to ‘‘that which bends up,’’ related to the debilitating polyarthralgia that most chikungunya patients experience. The polyarthralgia is usually symmetric and involves multiple joints, most frequently the hands, wrists, and ankles. High grade fever, up to 1048F, and severe malaise are also commonly described. Skin manifestations can be seen in 40% to 75% of patients and represent a wide range of pathology. The most common skin finding is a morbilliform rash, which can become confluent. In male chikungunya patients with skin involvement, 24% of patients developed aphthous-like ulcers in the scrotal region. This finding is associated with scrotal erythema and pain and swelling of the scrotum and groin. Nasal hyperpigmentation and vesiculobullous lesions have also been reported. Very rarely, purpuric patches have been reported as a cutaneous finding of chikungunya infection. Finally, the virus can cause an exacerbation of a patient’s underlying dermatoses. Worsening of psoriasis, tuberculoid leprosy, acne, and atopic dermatitis have all been reported. Chikungunya can be diagnosed by serology, viral culture, or PCR. Treatment options are only supportive at this time; however, a preventative vaccine is currently in phase I trial at the National Institutes of Health.
Comment: We present this case to highlight the disseminated appearance of herpes simplex virus in the immunocompromised. Widespread lesions are well documented in patients with eczema in the form of eczema herpeticum. Disseminated disease in patients with underlying systemic immunosuppression is a rare presentation. Widespread lesions with herpetic morphology in patients with a history or current status of immunosuppression should alert the physician to initiate antiviral therapy as therapy may inhibit systemic viral dissemination and produce rapid resolution of cutaneous lesions, as was noted in our patient.
Commercial support: None identified.
Commercial support: None identified.
1394 Herpes zoster child after intrauterine exposure to varicella-zoster virus Carmen Martınez Peinado, MD, UGC-Dermatologıa-CMA, Complejo Hospitalario de Jaen, Ja en, Spain; Ricardo Ruiz Villaverde, MD, PhD, Servicio de Dermatologıa del Hospital Virgen de las Nieves de Granada, Granada, Spain; Manuel Galan Gutierrez, MD, PhD, UGC-Dermatologıa-CMA, Complejo Hospitalario de Jaen, Jaen, Spain; Cristina Garrido Colmenero, MD, Servicio de Dermatologıa del Hospital Virgen de las Nieves de Granada, Jaen, Spain; Casto Martos Paredes, MD, PhD, Servicio de Pediatrıa del Centro de Salud Federico del Castillo de Jaen, Spain; Concepci on Sierra Corcoles, MD, PhD, Servicio de Pediatrıa del Complejo Hospitalario de Jaen, Jaen, Spain; Paloma Nogueras Morillas, MD, Servicio de Dermatologıa del Hospital Virgen de las Nieves de Granada, Granada, Spain Varicella zoster virus (VZV) is a neurotropic herpes virus that causes two distinct diseases. Varicella results from its primary infection. However, herpes zoster (HZ) is caused by reactivation of VZV resulting by the migration of the virus from the dorsal root ganglion along the neural pathways to the skin causing unilateral vesicular rash which usually is limited to a single or rarely two adjacent dermatomes. The appearance of HZ in a child without a history of varicella is rare and it may happen when the mother has had the disease during pregnancy. It happens usually from the first year of life, when maternal immunoglobulin G (IgG) disappears from his blood. Case report: A 6-year-old-healthy child without known drug allergies was referred to our hospital for an acute and painful rash that which clinical diagnosis was consent with impetigo. He did not improve with topical antibiotics and corticosteroids. As the background, we highlight his mother had varicella at week 30 during her gestation. The immunization schedule was correct but had not received the VZ antivaccine. Cutaneous examination revealed multiple tense blisters and clustered vesicles on an erythematous base, widely distributed right gluteus and sacral region, which also affected scrotal and perineal region, producing hydrocele. The lesions were metameric without crossing the midline, following the dermatomes from S1 to S4. It associates pain, fever and irritability. Clinical diagnosis of HZ was established and treatment began with intravenous acyclovir, analgesics and drying agents. Blood tests showed mild leukopenia with lymphocytosis and elevated CRP. The immunologic profile showed no abnormalities and serology revealed high titers of IgG anti VZV, being negative for HSV, CMV and HIV. Discussion: Child HZ is a rare entity and usually has a benign evolution. When it appears during the first months or years of life, with no personal history of the disease, it may suggest the existence of an intrauterine contact. The effects on the fetus of gestational varicella depend on the moment in which the infection occurs. There is a high risk of abortion or congenital varicella before 20 weeks’ gestation. If maternal infection is perinatal, the risk of neonatal varicella is high, due to poor development of the infant immune system. Between both periods, the fetus is born in most cases asymptomatic for the transfer of maternal IgG to control the infection, but once disappear it may appear an HZ. Commercial support: None identified.
J AM ACAD DERMATOL
1427 Purpura fulminans associated with acute West Nile viral encephalitis Laura Paul Fite, MD, Scott & White Memorial Hospital and Texas A&M Health Science Center School of Medicine, Temple, TX, United States; Palak Parekh, MD, Scott & White Memorial Hospital and Texas A&M Health Science Center School of Medicine, Temple, TX, United States Background: Purpura fulminans (PF) presents clinically as widespread purpura secondary to disseminated intravascular coagulation (DIC). It is due to deficiency or dysfunction of protein C or protein S. West Nile virus (WNV) is transmitted to humans through mosquito bites. Most individuals do not develop symptoms of West Nile fever and even fewer develop neuroinvasive disease. Rarely, WNV has been associated with a hemorrhagic fever syndrome. Case report: A 42-year-old male presented to the hospital with altered mental status and was found to have multiorgan failure and evidence of DIC. Shortly after hospital admission, he developed diffuse purpura which progressed to hemorrhagic bullae and eventually gangrene of all four extremities. Initial body fluid cultures were negative. Finally, the patient was diagnosed with acute West Nile viral encephalitis due to presence of immunoglobulin M and immunoglobulin G antibodies against WNV in the cerebrospinal fluid and serum. Skin biopsy specimen revealed epidermal necrosis and fibrin thrombi in blood vessels consistent with purpura fulminans. Discussion: Purpura fulminans is the clinical manifestation of DIC. It is most commonly associated with bacterial sepsis especially meningococcemia. PF can also occur in the neonatal period due to congenital deficiency of protein C or protein S. Previous studies have been able to demonstrate decreased levels of protein C associated with bacterial sepsis and autoantibodies against multiple coagulation proteins in postviral syndromes. Although rare, a similar case to this report, was recently published in the literature of a patient who developed diffuse purpura and multiorgan failure associated with acute WNV infection. It is suspected that host genetic factors may increase the risk for severe WNV disease. The morbidity and mortality rate is high especially due to development of symmetric peripheral gangrene leading to secondary infection and necessitating limb amputations. Conclusion: Purpura fulminans is an important to recognize dermatologic emergency. After diagnosis, it is essential to identify the underlying cause of DIC to determine the best treatment. PF is most commonly seen in acute bacterial sepsis but can be associated with WNV infection as reported here. Commercial support: None identified.