Herpes zóster en zona perianal y perineal en paciente pediátrico inmunodeprimido / Shingles perianal and perineal area in immunosuppressed paediatric patient

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Asociación serológica de la rinoneumonitis viral equina y la anemia infecciosa equina / Serological association between equine rinoneumonitis and equine infectious anemia viruses

Objetivo. Determinar el nivel de asociación serológica entre los herpesvirus equinos tipos 1 y 4 (HVE-1 y HVE-4) causantes de la rinoneumonitis equina y el virus de la anemia infecciosa equina (VAIE) en caballos de trabajo provenientes de 5 municipios del Meta. Materiales y métodos. Se realizó una encuesta serológica transversal en 68 equinos provenientes de los municipios de San Martín, Guamal, Restrepo, Cumaral y Paratebueno. Para la evaluación de los anticuerpos contra los HVE-1 y HVE-4, se utilizó un ELISA indirecto para detectar la presencia de anticuerpos dirigidos contra la glicoproteína G del HVE-1 y HVE-4 (Svanovir ™ EHV1/EHV4-Ab ELISA); para el diagnóstico de anticuerpos contra el VAIE se utilizó la prueba de inmunodifusión en agar de gel de Coggins. Resultados. No se encontraron reactores al HVE-1; sin embargo, el porcentaje de seropositividad fue de 94.12% (64/68) y 13.2%(9/68) para HVE-4 y VAIE respectivamente. El porcentaje de animales coinfectados HVE-4 y AIE fue 13.23% (9/68). Cuando se discriminaron los resultados por Municipio se encontró un 27.9% (19/68) de reactividad en el municipio de Restrepo, 26.5% (18/68) en Cumaral, 14.7% (10/68) en Paratebueno, 14.7% (10/68) en Guamal, y 10.3% (7/68) en San Martin. El porcentaje de reactores por municipio al VAIE fue Cumaral 5.88% (4/68), Restrepo 4.4% (3/68), Guamal 1.47%(1/68) y San Martín 1.47% (1/68). Conclusión. El alto porcentaje de coinfección entre HVE-4 y VAIE sugiere un efecto importante en la interacción, pues el efecto inmunosupresor del VAIE podría facilitar la reactivación del estado latente del HVE-4.

Comportamiento clínico y terapeutico del herpes zoster en el centro nacional de dermatología Doctor Francisco José Gómez Urcuyo enero 2002 - diciembre 2006 / Clinical and therapeutic behavior of herpes to zoster in center national of dermatology Doctor Francisco Jose Gómez Urcuyo January 2002 - December 2006

El Herpes Zóster es una infección producida por el virus Varicela - Zoster, siendo el único virus herpes capaz de producir dos cuadros diferentes: Varicela, como una enfermedad eruptiva de la infancia y Zóster, como una virosis de la edad adulta o de la senectud. En nuestro país, ha sido un problema poco estudiado y no se cuenta con investigaciones que reflejen el comportamiento real en el Centro Dermatológico Nacional "Dr. Francisco José Gómez Urcuyo", se realizó un estudio descriptivo, de corte transversal, no probalilístico con el objetivo de determinar el comportamiento clínico y terapéutico del Herpes Zóster. El universo lo conformaron 721 pacientes que fueron atendidos por primera vez en la consulta externa con diagnóstico de Herpes Zóster, la muestra fue constituida por 614 pacientes en los que se encontraron todos los datos completos. Dentro de los principales resultados, 326 pacientes fueron del sexo femenino y 286 masculinos. La gran mayoría de los pacientes (94 porciento) procedían del área urbana y sólo un 6 porciento eraan del área rural. 270 (45 porciento) fueron mayores de 50 años...

Infection in children with lupus nephritis receiving pulse and oral cyclophosphamide therapy.

Infection is the major complication of cyclophosphamide therapy in patients with lupus nephritis. The objectives of this study were to report and compare the rate of infection between children with lupus nephritis who had received intravenous pulse cyclophosphamide (IVCY) and those who had received oral cyclophosphamide (OCY) and to determine the risk factors for infection during treatment with cyclophosphamide in these groups. Records of nine patients who had received IVCY from the beginning [pure intravenous cyclophosphamide (PIVCY) group], 11 patients who had received prior oral cyclophosphamide and later switched to IVCY [combined intravenous cyclophosphamide (CIVCY) group] and 41 patients who had received OCY were reviewed. Infection occurred in 21 of 61 patients (34%). In the PIVCY group, four episodes of infection occurred in three of nine patients (33%). In the CIVCY group, six episodes of infection occurred in four of 11 patients (36%). In the OCY group, 18 episodes of infection occurred in 14 of 41 patients (34%). The rate of infection between these groups was not different (P=0.99). None of the following parameters were risk factors for infection: cumulative dose of cyclophosphamide, leukopenia and neutropenia. On the contrary, white blood cell (WBC) count and polymorphonuclear cell (PMN) count were significantly less in the no-infection group (P=<0.001, P<0.001, respectively), with odds ratios for leukopenia (WBCs <4,000 mm(3)) and neutropenia (PMNs <1,500 mm(3)) between the infection and the no-infection group equal to 0.18 (95%CI 0.05-0.63) and 0 (95%CI 0-0.19), respectively. Most of the patients who had infection received prednisolone at a dosage of more than 0.5 mg/kg per day (67% of the PIVCY group, 50% of the CIVCY group and 83% of the OCY group). Fatal infections occurred in two patients who had concomitant active systemic lupus erythematosus (SLE). Although lymphopenia (lymphocyte count <1,500/mm(3)) was not the risk factor for infection, it was observed that six of seven patients with herpes zoster had lymphopenia. Herpes zoster seemed to occur more frequently in the OCY group (15%) than in the whole IVCY group (5%), but there was no statistical difference (P=0.41). We conclude that the rate of infection in the IVCY and OCY group was not different. Infection is likely to occur in patients receiving a concomitant high dose of prednisolone. The occurrence of fatal infection in patients with active disease should be noted. No single risk factor was detected in this study.

[Granulomatous dermatitis following herpes zoster with detection of varicella zoster virus DNA]. / Postzosterische granulomatöse Dermatitis mit Nachweis von Varizella-Zoster-Virus-DNA.

The occurrence of a granulomatous inflammation following herpes zoster infection is uncommon and its pathogenesis is unclear. A 74-year-old male patient developed multiple red-brown papules following a secondary generalized infection with varicella zoster virus in the same area. The patient was suffering from a chronic lymphocytic B-cell leukaemia. Histopathologically, granulomatous dermatitis with multinucleate giant cells was found. Varicella zoster virus DNA was identified by polymerase chain reaction in the tissue. After a renewed antiviral therapy, skin lesions disappeared completely.

Prenatal diagnosis of congenital varicella infection.

Fourteen fetuses at risk of Varicella-Zoster virus (VZV) infection underwent prenatal diagnosis at 10-24 weeks' gestation by a combination of chorionic villus sampling, amniocentesis, and fetal blood sampling. Polymerase chain reaction (PCR) was done on fetal and placental tissues, using primers which define a 221 bp region of the gene coding for the 44 kD protein of VZV. Positive cases were further analysed by dot blot hybridization, using radiolabelled DNA probes corresponding to the Hind III fragment VZV genome. The rate of placental/fetal infection was 36 per cent (5/14 fetuses: 2/11 in the first and 3/3 in the second trimester). At post-mortem examination, two aborted fetuses had hydrocephaly and VZV DNA was found in most of the examined tissues. The nine women who tested negative at prenatal investigation delivered healthy neonates whose VZV-specific IgM antibody titres were negative and none of them developed herpes zoster infection. In view of the high frequency of fetal VZV infection and the reported low rate of malformations, the role of invasive prenatal diagnosis in women who acquire the infection in the first half of gestation is mainly that of reassurance when the test is negative.

Reactivated and latent varicella-zoster virus in human dorsal root ganglia.

Ganglia obtained at autopsy were examined by in situ hybridization from one patient with zoster (also called herpes zoster or shingles), two varicella-zoster virus (VZV)-seropositive patients with clinical evidence of zoster, one VZV-seronegative child, and one fetus. Ganglia positive for VZV had a hybridization signal in both neuronal and nonneuronal satellite cells. Ganglia obtained from the fetus and from the seronegative infant were consistently negative for VZV. Two striking observations were evident regarding the presence of VZV DNA in ganglia obtained from the individual with zoster at the time of death. First, ganglia innervating the sites of reactivation and ganglia innervating adjacent sites yielded strongly positive signals in neurons and satellite cells, whereas ganglia from distant sites were rarely positive. Second, VZV DNA was found in both the nuclei and the cytoplasm of neurons innervating areas of zoster. However, in neurons innervating zoster-free areas, VZV DNA was found only in the nucleus of neurons and their supporting satellite cells. Immunohistochemistry with a fluorescent monoclonal antibody to the VZV glycoprotein gpI, a late virus protein, revealed a positive signal in the cytoplasm of ganglia with clinical evidence of reactivation. These results illustrate that both neuronal and satellite cells become latently infected following primary VZV infection. The presence of VZV DNA and gpI in the cytoplasm of neurons demonstrates productive infection following reactivation at the site of latency.

Detection of latent varicella zoster virus DNA and human gene sequences in human trigeminal ganglia by in situ amplification combined with in situ hybridization.

Varicella zoster virus (VZV) establishes latency in sensory ganglia following primary infection (chickenpox) and may reactivate decades later to produce zoster (shingles). The presence of VZV DNA in latently infected ganglia has been demonstrated by Southern blot hybridization as well as by polymerase chain reaction of DNA extracted from latently infected ganglia. Conflicting results have been obtained by in situ hybridization studies to determine the cell type in the ganglia harboring the latent VZV. To address this controversy we have utilized a more sensitive method than the previous studies. We have applied the technique of polymerase chain reaction to sections of ganglia from latently infected individuals and combined this with in situ hybridization to detect the amplified product. Primers specific for VZV were used to amplify VZV DNA in latently infected human trigeminal ganglia and demonstrated the presence of VZV DNA in neurons only. Sections from human kidney and ganglia from neonates as well as monkey ganglia served as controls and did not show amplification of VZV sequences. Amplification using primers for human genes, alpha tubulin and the oncogene Bcl-2, demonstrated the presence of these sequences in nearly all cells in the human tissues while only weak signals were seen in the monkey tissue. This is the first report where in situ amplification has been utilized to detect latent VZV in human ganglia.

Varicella-zoster virus infection of the central nervous system in the acquired immune deficiency syndrome.

Productive varicella-zoster virus (VZV) infection of the central nervous system (CNS) was demonstrated in 11 acquired immune deficiency syndrome (AIDS) patients using immunocytochemistry and in situ hybridization. A characteristic zoster skin eruption was seen in only four cases. From our own series and 11 other cases in the literature, we identified five clinico-pathological patterns of VZV infection of the CNS in AIDS patients which could occur simultaneously. (i) Multifocal encephalitis predominantly involving the white matter, likely to be due to haematogenous spread of the infection was found in four cases. (ii) Ventriculitis was found in three cases. In two cases there was complete acute or chronic necrosis of the ventricular wall with marked vasculitis; in the third, the ependymal lining appeared irregular with foci of VZV-infected ependymal cells, some of which protruded into the ventricular lumen. (iii) Acute haemorrhagic meningo-myeloradiculitis with necrotizing vasculitis was observed in two cases. In one, this was associated with ventriculitis and was possibly due to shedding of infected ependymal cells into the ventricular lumen and secondary seeding of the CSF. (iv) Focal necrotizing myelitis was seen in one case. It followed cutaneous herpes zoster and was considered to result from neural spread from the diseased dorsal root ganglion similar to cases previously described of encephalitis limited to the visual system following VZV ophthalmicus, or bulbar encephalitis following a trigeminal zoster. (v) Vasculopathy involving leptomeningeal arteries and causing cerebral infarcts was seen in four cases, it was associated with meningitis in most cases. These findings are in keeping with the observation in non-AIDS patients that VZV spread to the CNS may follow different routes. Our study tends to show that VZV infection of the CNS occurs more frequently in AIDS than previously suspected and suggests that it must be considered as a diagnosis in cases of encephalitis, ventriculitis, focal myelitis, acute myeloradiculitis and cerebral infarcts in these patients.

Phenotypic and genotypic characterization of acyclovir-resistant varicella-zoster viruses isolated from persons with AIDS.

Phenotypic and genotypic analyses were done on 17 varicella-zoster virus (VZV) isolates recovered from 10 persons with AIDS (mean CD4 cell count, 16.4/mm3) who had chronic VZV lesions. Eleven acyclovir-resistant isolates were recovered from 10 patients after a mean of 20.1 weeks of therapy. Six susceptible isolates were recovered before acyclovir treatment (n = 1), early during therapy (n = 4; mean time, 4.2 weeks), or after discontinuation of acyclovir (n = 1). Acyclovir-resistant VZV isolates were deficient in thymidine kinase (TK) or induced a TK with altered substrate specificity; all isolates were susceptible to foscarnet. Ten of 11 acyclovir-resistant mutants contained tk gene mutations, including single nucleotide substitutions in highly conserved binding sites (n = 2) as well as nucleotide deletions (n = 4) and insertions (n = 4). These findings suggest that multiple, nonuniform mutations within the tk gene are associated with acyclovir-resistant VZV phenotypes.

Management of viral infections with thymopentin.

Recurrent herpes simplex-, herpes zoster- and human papilloma virus infections are sometimes difficult to control by traditional antiviral therapy. Although detectable immune disturbances are not regularly associated with the clinical presentation, a compromised cellular immunity has been found to play an important role in the pathogenesis of those diseases. Thymopentin (Arg-Lys-Asp-Val-Tyr) is a synthetic pentapeptide corresponding to the active structure of the natural 49 amino acids containing thymic hormone thymopoietin, which has shown impressive immunoregulatory activity in many animal model systems and human in-vitro tests. Cumulative clinical experience with this drug has suggested that it would be of particular value in certain recurrent viral diseases. This report summarizes some of the individual studies performed so far, and discusses the mechanisms of action within the context of relevant published articles in this field. Contrary to antiviral drugs, thymopentin's effect appears to be long-lasting also after discontinuation of treatment. The drug seems to be extremely safe and no serious adverse reactions have been reported to date.

Zoster sine herpete, a clinical variant.

Two otherwise healthy immunocompetent men, ages 62 and 66 years, experienced years of radicular pain without zoster rash. An extensive search for systemic disease and malignancy was negative. Varicella-zoster virus DNA, but not herpes simplex virus DNA, was found in the cerebrospinal fluid of the first patient 5 months after the onset of pain, and in the second patient 8 months after the onset of pain. Prolonged radicular pain without zoster rash combined with the presence of varicella-zoster virus in the cerebrospinal fluid indicates that both men had zoster sine herpete, and strongly supports this syndrome as a clinical variant.

Management of acyclovir-resistant herpes simplex and varicella-zoster virus infections.

Persons with AIDS who have CD4+ counts < or = 100 and transplant patients, especially bone marrow allograft recipients, may experience clinically significant infections with acyclovir-resistant herpes simplex virus (HSV) or varicella-zoster virus (VZV). Patients who have received prior repeated acyclovir treatment appear to be at the highest risk of harboring acyclovir-resistant strains. Algorithms for the management of these infections were developed at a recent roundtable symposium. The consensus of the panelists was that treatment with foscarnet should be initiated within 7-10 days in patients suspected to have acyclovir-resistant HSV or VZV infections. Foscarnet therapy should be continued for at least 10 days or until lesions are completely healed.

[Acute pancreatitis caused by varicella-zoster virus after liver transplantation]. / Pancréatite aiguë par le virus varicella-zoster après une transplantation du foie.

Twenty-six days after liver transplantation for primary biliary cirrhosis, a 52 year-old patient was rehospitalized for viral infection. The clinical features were fatigue, anorexia and vomiting. On physical examination, vesicular skin lesions involving the left 8 th intercostal space were suggestive of herpes-zoster infection. The following day the patient was extremely tired and dyspnoeic. The abdomen was distended with moderate abdominal epigastric pain. The clinical picture worsened rapidly and the patient died a few hours later. Autopsy revealed acute haemorrhagic necrosis of the pancreas due to herpes-zoster virus.

Tests for detecting herpes simplex virus and varicella-zoster virus infections.

Several laboratory diagnostic methods are available for the diagnosis, differentiation, and subtyping of HSV and VZV infections. In the office or at the bedside of a hospitalized patient, a positive Tzanck smear preparation is an inexpensive, rapid, and morphologic technique for confirming a suspected diagnosis of a herpesvirus infection. An expedient, slightly more expensive, reliable technique for establishing a HSV infection, yet not able to differentiate the subtype of that infection, is a recently marketed monoclonal antibody-based filtration type enzyme immunoassay (Kodak SureCell Herpes Test Kit). Serologic tests traditionally do not have a major role in the diagnosis of HSV infection; yet, new type-specific methods using Western blot assays may be useful for confirming the presence of unrecognized, subclinical HSV2 infections that are presently being underdiagnosed by current procedures. The gold standard for establishing the diagnosis of HSV infection has been the viral tissue culture. The fluorescent antibody to membrane antigen test and viral tissue culture have been the principal methods for diagnosing VZV infection. Immunomorphologic techniques have been useful adjuvant methods for both the diagnosis and the differentiation of HSV and VZV infections. Molecular virology techniques (particularly those using PCR) are likely to become the diagnostic methods of choice for both HSV infection and VZV infection once these tests become commercially available.

Detection of varicella-zoster virus DNA in conjunctivas of patients with herpes zoster.

Detection of varicella-zoster virus (VZV) DNA was carried out in the conjunctivas of 18 patients with herpes zoster by polymerase chain reaction. The rate of VZV DNA detection in conjunctivas was 3/4 in herpes zoster ophthalmicus associated with eruption on the dorsum nasi, 2/5 in herpes zoster ophthalmicus without eruption on the dorsum nasi, 1/2 in herpes zoster with eruption on the cheek and lower jaw, 1/2 in generalized herpes zoster and 0/5 in herpes zoster associated with eruption on the trunk or extremities, respectively. The reason for the detection of VZV DNA in conjunctivas is discussed.

Disseminated multifocal herpes zoster leukoencephalitis and subcortical hemorrhage in an immunosuppressed child.

We describe a rare case of multifocal varicella-zoster leukoencephalitis in an immunosuppressed adolescent boy who developed a herpetiform rash on his groin and subsequently presented with a subacute encephalopathy, aphasia, and hemiparesis. Magnetic resonance imaging scan of the brain revealed multifocal bi-hemispheric target-like lesions predominantly in the white matter. A magnetic resonance imaging scan 2 weeks later showed a subcortical hemorrhage in the left insular region. He received long-term high-dose intravenous acyclovir and had significant improvement in his neurologic status.

Herpes zoster: daily marking of new vesicles in therapeutic studies. A clinical method for objective assessment of the end of the eruptive phase.

BACKGROUND: The efficacy of a therapeutic agent must be evaluated by objective criteria. However, in herpes zoster (HZ) studies there has been no generally accepted objective clinical criterion. OBJECTIVE: Our purpose was to establish a clinical method for determining objectively the point in time at which the eruptive phase of HZ is completed (no new vesicle formation). This point is said to be a clinical criterion for the end of viral replication in the skin and thus for measuring the efficacy of a virustatic agent. METHODS: Newly formed vesicles were marked with differently colored permanent marker pens each day. This method was evaluated by comparing the results of acyclovir therapy in two groups of patients with HZ. (Group A, no underlying malignancy; n = 9. Group B, underlying malignancy; 64% of these patients were undergoing cytostatic polychemotherapy or had immunodeficiency; n = 22). RESULTS: In both groups, acyclovir stopped the eruption of new vesicles within 1.8 and 2.8 days, respectively (not statistically significant). Group B showed a tendency toward more protracted hematogenous dissemination and a longer duration of therapy. The total duration of the eruptive phase depended solely on the length of the interval between the onset of the HZ and the beginning of therapy. CONCLUSION: The method of marking new vesicles is independent of laboratory facilities, simple, and cost effective; in addition, this method is suitable for statistical evaluation. It is thus superior to other clinical methods for objective assessment of the progression of HZ.