Vesicular Skin Lesions Research Articles

Generalized vesicular skin lesions presented at birth in a newborn

Generalized vesicular skin lesions presented at birth in a newborn

Varicella-Like Cutaneous Toxoplasmosis in a Patient with Aplastic Anemia

A 60-year-old patient with aplastic anemia presented with vesicular varicella-like skin lesions on her face, arms, legs, back, and abdomen. However, diagnosis for herpetic infection was negative. Findings of a skin biopsy led to a tentative histologic diagnosis of toxoplasmosis, and infection with Toxoplasma gondii was confirmed by immunohistochemistry and PCR. Cutaneous toxoplasmosis is a rare finding in immunocompromised patients and might mimic other infectious diseases, and vesicular lesions associated with toxoplasmosis have not been reported previously.

Vernet Syndrome by Varicella-Zoster Virus

Vernet syndrome involves the IX, X, and XI cranial nerves and is most often attributable to malignancy, aneurysm or skull base fracture. Although there have been several reports on Vernet's syndrome caused by fracture and inflammation, cases related to varicella-zoster virus are rare and have not yet been reported in South Korea. A 32-year-old man, who complained of left ear pain, hoarse voice and swallowing difficulty for 5 days, presented at the emergency room. He showed vesicular skin lesions on the left auricle. On neurologic examination, his uvula was deviated to the right side, and weakness was detected in his left shoulder. Left vocal cord palsy was noted on laryngoscopy. Antibody levels to varicella-zoster virus were elevated in the serum. Electrodiagnostic studies showed findings compatible with left spinal accessory neuropathy. Based on these findings, he was diagnosed with Vernet syndrome, involving left cranial nerves, attributable to varicella-zoster virus.

247 Serial Cytokine Expressions in Infants with Incontinentia Pigmenti

BackgroundNF-kB dysfunction resulting from NEMO (NF-kappaB essential modulator) mutation can lead to significant alterations in cytokine production. However, little is known about changes in the expression of downstream molecules in...

Serial cytokine expressions in infants with incontinentia pigmenti

NF-κB dysfunction resulting from NEMO (NF-kappaB essential modulator) mutation can lead to significant alterations in cytokine production. However, little is known about changes in the expression of downstream molecules in patients with incontinentia pigmenti (IP). We aim to investigate serial cytokine expressions during the first 2 years of life in young infants with IP, the period in which skin inflammation and morphological changes are most significant. Gene analysis and X-inactivation test were performed for the two neonates with IP. Peripheral mononuclear cells were obtained after birth and successively at 6-month interval up to the age of two years. Levels of TNF-α and IL-6 were analyzed with ELISA before and after stimulating with Toll-like receptor ligands. The result showed the male IP patient had normal NEMO allele. His cytokine level, although initially lower, had returned to a level comparable with those of controls at 12 months of age. The female infant had mutated NEMO gene. Her baseline TNF-α level was significantly higher than those of the control subjects at birth and remained high by 6 months of age. All cytokine responses had decreased significantly by 2 years of age, the time in which all vesicular skin lesions had resolved. Both infants had normal serum immunoglobulin level and remained infection free during the follow up period. To our knowledge, this is the first report that demonstrates serial changes of cytokine profiles in humans with IP. This study showed that in the presence of NEMO mutation, alteration of cytokine production was remarkable during the first year of life, which may account for the prominent inflammatory changes in skin morphology.

Intrauterine Herpes Simplex Virus Infection in a Monochorionic Twin Gestation.

Herpes simplex virus (HSV) of the newborn affects 1 in 3200 [1] live births in the United States, and can be acquired by the intrauterine or intrapartum route, or postnatally. Intrauterine or congenital infection represents the rarest form (5% of cases) [2] and frequently has devastating consequences such as congenital brain malformation and severe neurocognitive impairment leading to fetal or neonatal death [3]. Here we present two cases of fatal intrauterine HSV infection in monochorionic twin infants. CASE A 21-year-old secundigravida mother with twin gestation of 26-4/7 weeks presented with spontaneous rupture of membranes of clear amniotic fluid 11 hours prior to delivery. She had negative prenatal laboratory studies for hepatitis B, syphilis, human immunodeficiency virus (HIV), and an unknown group B streptococcus status. Her sexually transmitted infection history included chlamydia trachomatis infection treated during early pregnancy and no history of HSV in herself or her sexual partner. A structural survey 1 week prior to delivery revealed severe hydrops and hydranencephaly in the first twin, and moderate hydrocephalus in the second twin. The mother was afebrile, well-appearing, and reported no history of recent illness or genital lesions before or during either of her pregnancies. Both mother and father refused HSV serologic testing. The first twin boy was delivered via cesarean section with Apgar scores of 1, 2, and 3, at 1, 5, and 10 minutes, respectively. The infant was apneic, unresponsive to resuscitation efforts, and died shortly after birth. On autopsy, gestation was shown to be monochorionic–monoamniotic, and the placenta had evidence of acute chorioamnionitis; however, it was not tested for the presence of HSV. The intracranial cavity was composed of hemorrhagic fluid and fragments of parenchymal tissue with extensive necrosis and chronic inflammation, consistent with meningoencephalitis, and the liver was calcified and necrotic. Viral immunostaining revealed the presence of HSV in the adrenal gland and brain parenchyma, and no virus was detected in the liver. No viral cultures were performed on autopsy tissue due to formalin fixation, and surface cultures for HSV were not performed. The second twin boy had Apgar scores of 5, 7, and 8 at 1, 5, and 10 minutes, respectively. He was immediately intubated for respiratory distress, received inotropes and intravenous fluids for hypotension, and was given ampicillin and gentamicin for presumed sepsis. At 5 hours of life, vesicular skin lesions on the neck were noted on physical examination (PE). PE was otherwise unremarkable. HSV studies were sent from the skin lesion (neck), mucosal surfaces (eyes, mouth, rectum), and cerebrospinal fluid (CSF), and empiric acyclovir 20 mg/kg every 8 hours was started. Initial white blood cell (WBC) count, platelet count, liver function, and serum electrolytes were normal. The CSF revealed 111 WBC/mm 3 with a lymphocytic predominance, 7600 red blood cells/mm 3 , protein 1245 mg/dL, and glucose 21 mg/dL. Blood and CSF bacterial cultures were sterile. Toxoplasma immunoglobulin M antibody, cytomegalovirus (CMV), and parvovirus B-19 polymerase chain reaction (PCR) yielded negative results. PCR was positive for HSV type 2 (HSV-2) and negative for HSV type l from all five tested sites.

Failure of the Smallpox Vaccine To Develop a Skin Lesion in Vaccinia Virus-Naïve Individuals Is Related to Differences in Antibody Profiles before Vaccination, Not After

Successful vaccination against smallpox with conventional vaccinia virus is usually determined by the development of a vesicular skin lesion at the site of vaccinia inoculation, called a "take." Although previous vaccination is known to be associated with attenuation of the take, the immunology that underlies a no-take in vaccinia-naïve individuals is not well understood. We hypothesized that antibody profiling of individuals before and after receiving vaccinia virus would reveal differences between takes and no-takes that may help better explain the phenomenon. Using vaccinia virus proteome microarrays and recombinant protein enzyme-linked immunosorbent assays (ELISAs), we first examined the antibody response in vaccinia-naïve individuals that failed to take after receiving different doses of the replication-competent DryVax and Aventis Pasteur (APSV) smallpox vaccines. Most that received diluted vaccine failed to respond, although four no-takes receiving diluted vaccine and four receiving undiluted vaccine mounted an antibody response. Interestingly, their antibody profiles were not significantly different from those of controls that did show a take. However, we did find elevated antibody titers in no-takes prior to receiving DryVax that were significantly different from those of takes. Although the sample size studied was small, we conclude the failure to take in responders correlates with preexisting immunity of unknown etiology that may attenuate the skin reaction in a way similar to previous smallpox vaccination.

Index of Suspicion in the Nursery

A 2.94-kg male infant is born at 39 weeks to a 19-year-old G1P0 woman. The pregnancy was complicated by gestational diabetes. The woman had no significant past medical history, including sexually transmitted diseases, and no significant family history. Prenatal screening for group B Streptococcus, Chlamydia, gonorrhea, syphilis, and human immunodeficiency virus were negative. Delivery is complicated by prolonged rupture of membranes for 18 hours, maternal fever (temperature of 38.9°C), and failure to progress. The baby is delivered in good condition by cesarean section. Apgar scores are 8 at 1 minute and 9 at 5 minutes. Vital signs are within normal limits, and physical examination at birth shows no abnormal findings of note. The infant is admitted to the newborn nursery for observation. Blood culture is drawn and empiric antibiotics are started. Hematologic parameters are within normal limits and C-reactive protein measures 0.5 mg/dL. Antibiotics are continued for suspected chorioamnionitis. He is otherwise feeding well, euthermic, and looking well, and his blood culture remains negative. On postnatal day 7, the nurse notices two vesicular skin lesions: one on the right side of the forehead (Fig. 1) and the other on the vertex of the scalp (Fig. 2). Both comprise groups of clustered tiny vesicles that have minimal erythema at their bases. Vital signs and physical examination findings are within normal limits. The result of a simple test supports the diagnosis, and further laboratory investigations confirm the cause. Figure 1. Vesicular lesions on the right side of the forehead. Figure 2. Vesicular lesions on the vertex of the scalp. # Case: Blister in a Baby: Benign or Bothersome? {#article-title-2} ### Differential Diagnosis Vesiculobullous lesions in neonates should never be ignored because the cause could range from benign, self-limited conditions to serious fatal diseases. Early diagnosis and management are crucial …

Poor neurological sequelae of herpes simplex virus encephalitis in an infant despite adequate antiviral and adjunct corticosteroid therapy

A 2-month-old infant presented to our emergency department with fever, altered consciousness, and focal seizures of acute onset. He had vesicular skin lesions over the right preauricular region. CT brain showed a large hypodense lesion involving the left temporo-parietal region, left basal ganglia and left thalamus. MRI brain revealed bilateral multifocal corticomedullary lesions suggestive of encephalitis. CSF-PCR was positive for herpes simplex virus (HSV) type I. He was treated with standard dose intravenous acyclovir for 15 days along with a trial of pulse methylprednisolone, but was readmitted within a week with features of an early relapse. The infant survived but developed significant neurological sequelae. Although treatment of HSV is available, the neurological outcome is guarded even with adequate antiviral therapy. Adjunct corticosteroid therapy did not appear to attenuate the neurological sequelae.

Varicella outbreak in Indian students in Magdeburg with detection of the African‐Indian VZV clade 5

Varicella has the highest contagiosity index of all viral diseases. We report an endemic outbreak of varicella among 4 Indian students in Magdeburg in November and December 2008. An initially severe course was observed in three of these patients with a negative vaccination status. Large vesicular skin lesions with a diameter of up to 8 mm were found in all patients. Molecular genetic tests revealed African/Indian clade 5 in 2 patients, although the European clades (i.e., clade 1 and 3) are the most common in Germany, accounting for 85 %. All patients recovered without any complications after administration of intravenous aciclovir at a dosage of 10 mg per kg body weight. Although isolated cases of varicella are not notifiable according to the German Protection against Infection Act, endemic outbreaks must be reported to the appropriate health surveillance authorities.

Incontinentia pigmenti revisited. A novel nonsense mutation of the IKBKG gene

To describe and evaluate the clinical and molecular findings of patients with incontinentia pigmenti (IP) in Greece. We examined 12 female patients, initially aged 2 weeks to 7 months with clinical diagnosis of IP. Standard tests were performed including skin biopsies and ocular, dental and neurologic examinations. Molecular analysis was carried out on 8 out of 12 cases. The initial clinical examination was stage 1 (vesicular lesions), stage 2 (verrucous lesions) or stage 3 (hyperpigmented linear lesions of the trunk/limbs). At the final clinical examination, 10 of our patients had typical vesicular, verrucous or mixed hyper-hypopigmented skin lesions which had persisted from the neonatal period; seven had delayed dentition or conical teeth; two had developmental delay; one had microcephaly and strabismus and two had scarring alopecia. In seven patients, deletion of exons 4-10 of the IKBKG gene was found. In one patient, skewed X-inactivation was demonstrated and a novel mutation p.Gln332X was found. The mothers' DNA analyses were all normal. In our sample, all the cases were sporadic and the diagnosis of IP was based mainly on clinical features and confirmed with skin histology. Molecular analysis was used to find the mutations, in some cases to confirm diagnosis and to identify the carriers, which are crucial for prenatal and preimplantation diagnosis.

Rickettsia africaeInfection in Man after Travel to Ethiopia

To the Editor: The first human case of African tick-bite fever was described in 1992 as occurring in Zimbabwe. The causative agent was identified as a new serotype of the spotted fever group (SFG) rickettsiae and named Rickettsia africae (1). These findings confirmed observations made by Pijper in the 1930s, which suggested that there were 2 different kinds of human SFG rickettsioses in sub-Saharan Africa: Mediterranean spotted fever caused by R. conorii and transmitted by Rhipicephalus species, ticks of dogs, and African tick-bite fever caused by R. africae and transmitted by Amblyomma species, ticks of cattle and wild ungulates. African tick-bite fever has subsequently been diagnosed in patients from several other sub-Saharan countries and also from the West Indies (2,3). In a recent analysis of the spectrum of diseases among returning travelers, tick-borne spotted fever was (after malaria) the second most frequent cause of systemic febrile illness among those returning from sub-Saharan Africa. It occurred more frequently than typhoid fever and dengue fever (4). The following case description reports an infection with R. africae in a man in France who recently returned from Ethiopia. On November 4, 2005, a 62-year-old French man sought care at the Medical Center of the Institut Pasteur in Paris for fever, along with chills, headache, neck and shoulder pain, and fatigue over the previous 4 days. At the onset of these symptoms he had noticed dark nodular lesions on his neck and his left groin followed 2 days later by a slightly painful eruption on his arms and his trunk. He had spent a month in southwest Ethiopia, north of Kelem near the Sudanese border, and returned to France on October 26, 2005. While in Ethiopia, he had assisted with a production of a documentary film about an Ethiopian tribe and had been in contact with cattle in the villages. He had not noticed any tick bites. On physical examination he had a fever of 38°C, a nodular lesion with a central dark crust on his neck, a second lesion on his left inguinal fold (Figure, panel A), and a vesicular eruption on his arms and his trunk (Figure, panel B). Leukocyte count was 3,200, including 1,869 neutrophils and 867 lymphocytes. The platelet level was 174,000/mm3. The C-reactive protein level was 28.3 mg/L. The aspartate aminotransferase level was slightly elevated. The patient was treated with doxycycline 200 mg/day for 1 week for suspected African tick-bite fever. Follow-up showed a quick recovery from his symptoms except for fatigue that persisted for ≈1 month. Figure Inoculation eschar on left inguinal fold (A) and vesicular skin lesion (B) in a traveler recently returned to France from Ethiopia. A commercial immunofluorescence assay for R. conorii and R. typhi immunoglobulin G performed both on an initial blood sample and a second sample taken 1 week later were negative. A blood sample and a biopsy specimen of the inguinal eschar were sent to the National Reference Center of Rickettsiae in Marseille, France. Although cellular culture of both specimens and molecular testing of the blood sample were negative, PCR for the sequences of citrate synthase (GenBank accession no. {type:entrez-nucleotide,attrs:{text:RAU59733,term_id:1389980}}RAU59733, 93.1% homology) and rickettsial OmpA (GenBank accession no. {type:entrez-nucleotide,attrs:{text:RAU83436,term_id:62861416}}RAU83436, 99.3% homology) applied on the skin biopsy detected R. africae and confirmed the diagnosis of African tick-bite fever. From 1969 to 1971, SFG rickettsiae were isolated from Amblyomma spp. ticks collected in Ethiopia. They were regarded as R. conorii or as closely related bacteria (5). Later, more specific tests using western immunoblots with monoclonal antibodies showed that these rickettsiae differed from R. conorii (6). In 1992 SFG rickettsiae isolated from Amblyomma ticks collected in Zimbabwe and from the blood of a patient in Zimbabwe were compared to R. conorii, to other pathogenic SFG rickettsiae, and to a SFG rickettsia isolated from an Amblyomma spp. tick in Ethiopia 20 years before. The SFG rickettsia isolates from Ethiopia were identical to isolates obtained in Zimbabwe from the Amblyomma ticks and the patient’s blood and were different from R. conorii and other pathogenic SFG rickettsiae. This new serotype of SFG rickettsiae was named R. africae (1,7). A recent study confirmed the presence of R. africae in ticks collected in Ethiopia, as well as R. aeschlimanii (8). Thus, evidence of R. africae in Ethiopia has been known for a long time. The geographic distribution of African tick-bite fever is related to the presence of Amblyomma spp. ticks, vectors and reservoirs of R. africae. Consequently African tick-bite fever should also be considered as a possible diagnosis in patients with febrile illness returning from countries where R. africae has been detected in Amblyomma ticks, even if a human infection has not yet been reported (9,10).

Herpes Simplex

Herpes Simplex

A new generic real-time reverse transcription polymerase chain reaction assay for vesiviruses; vesiviruses were not detected in human samples

Different viruses belonging to the genus Vesivirus infect a broad range of animals, and cause gastroenteritis, vesicular skin lesions, hemorrhagic disease, respiratory diseases and other conditions. A recent report on Vesivirus viremia, as detected by PCR, in samples from patients with hepatitis of unknown etiology in the USA suggested a zoonotic potential for vesiviruses. These results have not been confirmed by another laboratory. In order to do so, a generic PCR assay on the RNA polymerase region was developed, and validated with RNA from 69 different Vesivirus species. Except SMSV serotype-8, all species tested were detected, including the ones that were suggested to be involved in zoonotic transmission in the USA (SMSV serotype-5). The generic Vesivirus assay was used on RNA extracted from serum samples from patients with hepatitis, stool samples from patients with gastroenteritis, throat-swab specimens of patients with rash illnesses, throat-swab and nose-swabs of patients with acute respiratory diseases, and cell cultures with cytopathologic effect from enterovirus surveillance in which no pathogen was found. None were found positive. In this study a generic Vesivirus assay was developed and it was concluded that vesiviruses are an unlikely cause of common illnesses in humans in the Netherlands.

The value of Tzanck smear test in diagnosis of erosive, vesicular, bullous, and pustular skin lesions

Tzanck smear is generally used for the diagnosis of the pemphigus group of autoimmune bullous diseases and mucocutaneous herpesvirus infections. There are only a few studies in the literature investigating its diagnostic value. We aimed to investigate Tzanck smear findings and to determine the diagnostic value of this test in moist (erosive, vesicular, bullous, and pustular) skin lesions. We also aimed to develop an algorithmic approach for the diagnosis of these types of skin lesions according to the Tzanck smear findings. Samples were stained with May-Grünwald-Giemsa and evaluated by the same dermatologist. In some patients, methylene blue and Gram staining or direct immunofluorescence examinations were additionally performed. In all of the study cases, after the evaluation of clinical and laboratory findings (including, when appropriate, potassium hydroxide examination; viral serology; bacterial and fungal cultures; histopathology; direct and indirect immunofluorescence; patch testing), the definite diagnosis was established. We also determined the sensitivity and the specificity of certain Tzanck smear findings. Tzanck smear was performed in a total of 400 patients with moist skin lesions. The sensitivities of multinucleated giant cells and acantholytic cells in herpetic infections, dyskeratotic acantholytic cells and cocci in bullous impetigo, pseudohyphae in candidiasis, acantholytic cells in pemphigus and more than 10 tadpole cells (magnification x100) in spongiotic dermatitis were 84.7%, 92%, 100%, 100%, and 81.5%, respectively. Because Tzanck smears were evaluated by the same dermatologist, no comment could be made regarding the interobserver reliability of this test and how the level of experience with this technique might affect the results. Also, the sensitivity and the specificity of Tzanck smear test findings for certain diseases could not be calculated because of an insufficient number of patients. The Tzanck smear test is an inexpensive, useful, and an easy diagnostic tool for certain skin diseases.

Tularemia with Vesicular Skin Lesions May be Mistaken for Infection with Herpes Viruses

Tularemia with Vesicular Skin Lesions May be Mistaken for Infection with Herpes Viruses

Tularemia with Vesicular Skin Lesions May Be Mistaken for Infection with Herpes Viruses

The original reports of human infection with Francisella tularensis noted vesicular skin rash as a manifestation. We present 2 cases of tularemia initially diagnosed as herpes simplex or varicella zoster infection. Clinicians must recognize the cutaneous manifestations of tularemia and be able to distinguish these from lesions seen with herpes viruses.

Cutaneous anthrax in Eastern Turkey: a review of 85 cases

Anthrax is a zoonotic disease diminishing worldwide. Although a very rare disease in developed countries, anthrax is still endemic in developing countries. To evaluate the clinical history and features, treatment and outcome of our patients with anthrax and emphasize the importance of the disease in our region. In this study, the records of all patients diagnosed with cutaneous anthrax admitted to Yüzüncü Yil University Medical Faculty between March 2002 and March 2007, were reviewed, and data on age, gender, occupation, clinical symptoms and findings, location and type of lesions, clinical history, laboratory findings, treatment and outcome were recorded. There were 85 patients [46 (54.1%) male, 39 (45.9%) female; mean age 30.6 years, range 6-72]. All the patients had a history of contact with infected animals or animal products. The infectious agent was found using direct examination of Gram-stained smears from 17 patients (20%), and Bacillus anthracis was isolated from vesicle fluid cultures from 11 patients (12.9%). Diagnosis was based on clinical findings in the remaining 57 patients (67.1%). All patients, except for two with respiratory tract obstruction, made a full recovery. Anthrax continues to be an endemic disease in Turkey, and should be considered in patients with a relevant contact history having a painless ulcer and vesicular skin lesions surrounded by a zone of oedema. Gram staining and simple culture methods are useful aids to diagnosis, but diagnosis may have to be based on clinical grounds in the majority of patients.

Visual Diagnosis

1. Lopa Shah, MD* 2. Gita Balakumar, MD* 1. *University of Nevada School of Medicine, Las Vegas, Nev A 3-week-old girl presents to the clinic for a persistent rash that has been present since birth. Following an uncomplicated term gestation, the infant was born by cesarian section due to prolonged dilation and failure to progress. She weighed 3.2 kg. A rash was noted at birth on her left lower extremity, and her parents were reassured that the rash would resolve. However, the rash now extends over both lower extremities. The mother has not applied any creams, lotions, or topical medications to the infant’s skin. The family history is noncontributory; there is no history of nervous system or skin disorders. The infant is well-appearing, comfortable, and afebrile. She weighs 3.54 kg (25th percentile). Skin examination reveals red, hyperpigmented streaks and plaques on the upper part of her lower extremities (Fig. 1), with occasional vesicles distributed linearly (Fig. 2). An accessory nipple is noted on the right chest wall. The infant is active, there is no evidence of scratching, and her muscle strength and tone are normal for age. The remaining physical findings are normal. Figure 1. Red, hyperpigmented streaks and plaques on left lower extremity. Figure 2. Vesicles on left lower extremity. A complete blood count demonstrates: hemoglobin, 12.5 g/L (125 g/L); white blood cell count, 46.3×103/mcL (46.3×109/L) with 14% neutrophils, 2% bands, 33% lymphocytes, 44% eosinophils, and 1% myelocytes; and platelet count, 560.0×103/mcL (560.0×109/L). Peripheral blood smear reveals a slight normochromic, normocytic anemia with erythropenia, normal red cells with a few teardrop cells, moderately increased number of platelets, and a mild-to-moderate increase of white blood cells with relative and absolute eosinophilia. A clinical diagnosis is made. The presence of vesicular and hyperpigmented linear skin lesions since birth, their distribution over lines of Blaschko, and the laboratory finding of …

Avipoxvirus Infection in a Collection of Captive Stone Curlews (Burhinus oedicnemus)

A natural outbreak of avipoxvirus occurred in recently purchased stone curlews (Burhinus oedicnemus) at a breeding farm and subsequently spread to other stone curlews residing at the farm. The initial outbreak was characterized by mild vesicular skin lesions on the legs, which then developed crusts and bled. The overall morbidity rate was 100%, but none of the birds died, and all recovered without complication. Four gallinaceous species, also kept on the farm, did not develop lesions. Avipoxvirus was identified from the skin lesions by virus isolation, electron microscopy, and monoclonal antibody testing, as well as by polymerase chain reaction testing. Eight months after this outbreak, 7 male stone curlews developed large, round, crusty lesions on their legs. Although poxvirus virions were identified in the lesions, results of virus isolation were negative. These lesions possibly were the result of a recrudescence of the original infection in male birds that were stressed because they were housed together during the breeding season. This is the first clinical description of an avipoxvirus infection in stone curlews.