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PubMed2002

Enterovirus infections: a review of clinical presentation, diagnosis, and treatment.

The enteroviruses, RNA viruses of the Picornaviridae family, are ubiquitous pathogens which include more than 70 different serotypes that infect people of all ages and tend to occur seasonally in the summer and fall. Clinical manifestations may vary diversely with one serotype, while multiple serotypes can present with identical symptoms and may mimic bacterial infections. Most enterovirus infections cause benign, self-limiting disease; however, they can also produce severe and sometimes fatal illnesses such as meningitis, encephalitis, myocarditis, neonatal sepsis, and polio. Severe enterovirus infections are being diagnosed and treated earlier with better prognostic outcomes due to the advances of polymerase chain reaction technology in accurately detecting virus in patient fluids as well as the recent development of new antiviral therapies.

Enterovirus Infections↗
PubMed1995

A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM. Childhood Diabetes in Finland (DiMe) Study Group.

Coxsackievirus B infections have been associated with clinical manifestation of insulin-dependent diabetes mellitus (IDDM) in several studies, but their initiating role in the slowly progressing beta-cell damage is not known. This is the first prospective study designed to assess the role of coxsackie B and other enterovirus infections in the induction and acceleration of this process. Three separate series were studied: 1) an intrauterine exposure series comprising 96 pregnant mothers whose children subsequently manifested IDDM and 96 control mothers whose children remained nondiabetic; 2) a cohort of 22 initially unaffected siblings of diabetic children who were followed until they developed clinical IDDM (mean observation time, 29 months) and 110 control siblings who remained nondiabetic; 3) a case-control series comprising 90 children with newly diagnosed IDDM and 90 control subjects. Enterovirus infections were identified on the basis of significant increases in serum IgG, IgM, or IgA class antibodies against a panel of enterovirus antigens (capture radioimmunoassay). Enterovirus antibodies were significantly elevated in pregnant mothers whose children subsequently manifested IDDM, particularly in cases in which IDDM appeared at a very young age, before the age of 3 years (P < 0.005). Serologically verified enterovirus infections were almost two times more frequent in siblings who developed clinical IDDM than in siblings who remained nondiabetic (mean, 1.0 vs. 0.6 infections/follow-up year; P < 0.001). This difference was seen both close to the diagnosis of IDDM and several years before diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1990

Persistent enterovirus infection in culture-negative meningoencephalitis: demonstration by enzymatic RNA amplification.

Chronic meningoencephalitis due to enterovirus infection can occur in patients with antibody deficiencies. A modified polymerase chain reaction technique demonstrated persistent echovirus 11 infection in such a patient, despite negative routine viral cultures and negative routine nucleic acid hybridization. Although the sequence of echovirus 11 has not yet been determined, genomic conservation among the enteroviruses is significant, permitting detection of echovirus 11 with a primer pair and probe derived from enterovirus serotypes that have been fully sequenced. This study provides the first definitive evidence for the persistence of enterovirus infection with negative viral cultures.

Agammaglobulinemia↗
PubMed2004

Presentation, diagnosis, and management of enterovirus infections in neonates.

The nonpoliovirus enteroviruses commonly infect newborns, with consequences ranging from asymptomatic infection and benign illness, to severe, life-threatening disease. Frequently occurring symptoms include fever, irritability, lethargy, anorexia, and rash. Although most illnesses are mild, severe disease develops in a subset of newborns infected in the first 2 weeks of life. Severe disease may consist of sepsis, meningoencephalitis, myocarditis, pneumonia, hepatitis, and/or coagulopathy. Substantial mortality rates have been reported, and long-term sequelae may occur among survivors. Risk factors and clinical features associated with severe disease include absence of neutralizing antibody to the infecting serotype, maternal illness prior to or at delivery, prematurity, illness onset within the first few days of life, multiorgan disease, severe hepatitis, positive serum viral culture, and specific infecting serotype (e.g. group B coxsackieviruses and echovirus 11). Whereas the mainstay of diagnosis has traditionally been viral isolation in tissue culture, the polymerase chain reaction has been demonstrated to be more sensitive than culture, highly specific, and rapid. Immunoglobulin has been used as a therapeutic agent for neonates with enterovirus disease; however, clinical efficacy has not been proven. Specific antiviral therapy for enteroviruses is in development. Pleconaril is an investigational agent that inhibits viral attachment to host cell receptors and uncoating of viral nucleic acid. It has broad and potent anti-enterovirus activity, excellent oral bioavailability, and is well tolerated. Some clinical trials have demonstrated benefit in children and adults with enterovirus meningitis, and in adults with upper respiratory tract infections caused by picornaviruses (rhinoviruses or enteroviruses). Data summarizing compassionate use for severe enterovirus diseases (including neonatal sepsis) also suggest possible benefit. Limited pharmacokinetic data are available in infants and neonates. A multicenter, placebo-controlled, randomized trial of pleconaril in neonates with severe hepatitis, coagulopathy, and/or myocarditis is currently being conducted.

Adult↗
PubMed2003

Enterovirus infection may induce humoral immune response reacting with islet cell autoantigens in humans.

Molecular mimicry is one of the mechanisms by which enterovirus infections have been postulated to have a role in the pathogenesis of type 1 diabetes. Immunogenic epitopes in enterovirus capsid protein VP1 and procapsid protein VP0 have sequence similarities with diabetes-associated epitopes in tyrosine phosphatase IA-2/IAR and heat shock protein 60. In the present study, documented enterovirus infection was shown to induce humoral responses, that in 7% and 1% of patients cross-reacted with the known diabetes-associated epitopes in tyrosine phosphatase IAR and heat shock protein 60, respectively. In contrast, none of the children vaccinated against poliomyelitis had antibodies to the diabetes-associated epitope of tyrosine phosphatases IA-2/IAR. The antibody response studied in serum samples from six patients with coxsackievirus A9 infection was mainly targeted to capsid protein VP1. Coxsackievirus A9 infection induced antibodies cross-reacted with one epitope in heat shock protein 60, but not with epitopes derived from other autoantigens. Most diabetic children had high levels of antibodies to both coxsackievirus and poliovirus derived VP1 peptides but the pattern of reactivity did not differ from that seen in healthy children. The reactivity of linear epitopes derived from autoantigens was low in general and associated with the presence of multiple autoantibodies in the patients. Some linear auto-epitopes derived from tyrosine phosphatase IA-2, glutamic acid decarboxylase 65, preproinsulin, and heat shock protein 60 were recognized by sera from diabetic patients, but not by sera from healthy children. In conclusion, enteroviruses may induce immune responses that react with islet cell autoantigens, which is a concern when a putative inactivated enterovirus vaccine is considered.

Adolescent↗
PubMed1996

Enterovirus infection of the central nervous system of humans: lack of association with chronic neurological disease.

We have searched, using a sensitive nested-PCR, for enterovirus RNA in cerebrospinal fluid and post mortem central nervous system (CNS) tissue from patients with previous poliomyelitis with or without late functional deterioration, patients with motor neuron disease (MND), and control patients with other neurological disease or without neurological disease. Enterovirus RNA was detected in patients with previous poliomyelitis and MND, but also in control patients with and without neurological disease. Our results do not provide any evidence that such enterovirus infection is related to late functional deterioration in patients with previous poliomyelitis, which could be attributed to other medical conditions in most instances, and do not support the hypothesis that MND is associated with enterovirus infection of the CNS. Nucleotide sequence analysis of enterovirus RNA sequences detected indicated that enteroviruses detected were of the non-polio type.

Adult↗
PubMed2005

Diagnosis and outcomes of enterovirus infections in young infants.

BACKGROUND: Enterovirus (EV) infections commonly cause fever in infants younger than 90 days of age. The polymerase chain reaction (PCR) has improved our ability to diagnose EV infections. OBJECTIVE: To evaluate the utility of blood and cerebrospinal fluid (CSF) specimens for the diagnosis of EV infections by PCR and to describe a large cohort of EV-infected infants. DESIGN/METHODS: Febrile infants younger than 90 days of age evaluated for sepsis at Primary Children's Medical Center in Salt Lake City, UT, were enrolled in a prospective study designed to identify viral infections from December 1996 to June 2002. All patients had bacterial cultures of blood, urine and CSF. Testing for EV was performed by PCR and/or viral cultures. Patients who were positive for EV were identified for this study. RESULTS: Of 1779 febrile infants enrolled, 1061 had EV testing and 214 (20%) were EV-positive. EV infections were diagnosed by PCR of blood, CSF or both in 93% of infants. PCR testing was positive in blood in 57%, and blood was the only positive specimen for 22% of EV infected infants. PCR of CSF was positive in 74%. The mean age of infants with EV infection was 33 days, with 18% younger than 14 days and 5% younger than 7 days. Fifty percent of EV-positive infants had CSF pleocytosis. Of EV PCR-positive infants, 91% were admitted, and 2% required intensive care. Possible serious EV disease was diagnosed in <1%, and there were no deaths. Twelve infants (5.6%) had concomitant urinary tract infection, and 3 (1%) had bacteremia. CONCLUSIONS: EV infections are common in febrile infants younger than 90 days. Blood and CSF are equally likely to yield positive results by PCR, but the combination of both specimens improved the diagnostic yield.

Blood↗
PubMed1991

Focal encephalitis with enterovirus infections.

We report on four pediatric patients with Enterovirus infections who were admitted to the hospital with signs or symptoms of acute, focal encephalitis. All four experienced focal seizures. Each had a cerebrospinal fluid pleocytosis at the initial lumbar puncture. In all four patients the diagnosis of herpes simplex encephalitis was entertained. Each child improved spontaneously within a few days of admission to the hospital, and only one had residual neurologic abnormalities at the time of discharge. A brief review of these cases, and three additional cases from the literature, indicate that the enteroviruses, particularly the group A Coxsackieviruses, are rare causes of acute focal encephalitis in children and adolescents.

Adolescent↗
PubMed1995

Diagnosis of neonatal enterovirus infection by polymerase chain reaction.

A 5-hour colorimetric polymerase chain reaction (PCR) assay was more sensitive than viral culture in identifying viral infection in initial serum (13/16 vs 5/16; p = 0.008) and urine (10/16 vs 5/16; p = 0.2) specimens from 16 enterovirus-infected newborn infants, and remained more sensitive throughout their illnesses. Combined sensitivity of serum and urine PCR was 14 of 16 (88%). Results of all acute-phase PCR assays of serum and urine from four neonates with cultures negative for enterovirus were also negative. PCR assay of serum and urine facilitates rapid, accurate diagnosis of neonatal enterovirus infections.

Enterovirus↗
PubMed2002

Enterovirus infection during pregnancy is not a risk factor for celiac disease in the offspring.

BACKGROUND: There is a strong genetic influence on the susceptibility to celiac disease but it is also evident that environmental factors play a role in the development of the disease. Diverging studies about adenovirus infection as a possible triggering factor in the pathogenesis have been reported. Our study was undertaken to determine whether enterovirus infection during pregnancy is a risk factor for the development of celiac disease later in childhood. METHODS: Cord blood from 76 mothers whose children developed celiac disease before 15 years of age were analyzed for IgA, IgG, and IgM antibodies for enteroviruses and Ig-A endomysium antibodies. The control group comprised cord blood from 327 mothers with children without known celiac disease. RESULTS: There were no significant differences in antibody titers for enterovirus between the two groups. IgA-endomysium antibodies were elevated in 3 of the 76 mothers, whereas none had known celiac disease. CONCLUSION: This study does not show that enterovirus infection during pregnancy is associated with the development of celiac disease in childhood. Of the mothers whose children developed celiac disease, 4% had Ig-A endomysium antibodies, which may reflect a silent celiac disease.

Adolescent↗
PubMed1993

[Enterovirus infections].

Non-polio enteroviruses are currently the most common agents of the central nervous system viral infection, and are the major causes especially in patients with aseptic meningitis. The practical problems with enterovirus meningitis revealed from the investigation of our patients are as follows. (1) The triad of symptoms of meningitis (fever, headache, vomiting) were seen only in 50% of the older children affected. The only manifestation of neonates with aseptic meningitis was fever. (2) In more than half of the patients, the cerebrospinal fluid showed polymorphonuclear predominance within 3 days from the onset. (3) The causal viruses were isolated frequently (70%) from the cerebrospinal fluid of the children with aseptic meningitis. (4) The patients more than 1 year of age had no sequela clinically. Among neonates and early infants, transient abnormalities of brain CT findings were seen in 40% and delayed speech in 30%. Their prognosis should be investigated more precisely.

Enterovirus Infections↗
PubMed1990

Secondary enterovirus infection in the murine model of myocarditis. Pathologic and immunologic aspects.

Enteroviruses are implicated as etiologic agents in the inflammatory diseases myocarditis and polymyositis. In this report, we show that a previous enterovirus exposure in mice can influence development of myocardial inflammation with a second enteroviral exposure. Inoculation of 25-day-old male C3H/HeJ mice with 10(3) or 10(5) plaque-forming units (PFU) of infectious or ultra violet (UV)-inactivated coxsackievirus B2 (CVB2), followed by inoculation 28 days later with 10(5) PFU of a myocarditic variant of coxsackievirus B3 (CVB3-m) results in more intense myocardial inflammation and injury than is seen in age-matched mice inoculated with CVB3-m alone. More severe disease occurs with the lower primary dose of CVB2. Neutralizing antibody to CVB2 is detected early after primary inoculation and neutralizing antibody to CVB3 is first detected 5 days after secondary inoculation. In vitro proliferation of splenocytes from mice inoculated with one or both viruses occurs in response to both CVB2 and CVB3 antigens. We recently demonstrated that murine T cells are capable of recognizing an enterovirus group antigen. Thus cell-mediated immune responses to a conserved antigenic epitope(s) among the enteroviruses may be involved in the exacerbation of myocardial inflammatory disease during a second enterovirus infection. The secondary infection model described here may more accurately mirror virus-induced myocarditis in the human population because the majority of adults have been exposed to several enteroviruses before induction of disease.

Animals↗
PubMed1998

Enterovirus infections as a possible risk factor for myocardial infarction.

BACKGROUND: An increasing body of evidence suggests that, in addition to the well-known classic risk factors, some microbial infections may be associated with the development of atherosclerosis and myocardial infarction (MI). The aim of our study was to evaluate the possible role of enteroviral infections in the pathogenesis of MI. METHODS AND RESULTS: Stored sera, collected in Eastern Finland in 1977, from a set of 12 155 randomly selected men and women aged 25 to 64 years were used in prospective, nested case-control study. The study sample comprised 183 men and 81 women with MI and matched controls. The sera were tested for IgG antibodies to a newly identified enterovirus-common (EVC) antigen, to heat-denatured coxsackievirus B5 (CBV-5), and to adenovirus hexon protein. Raw data from enzyme immunoassays were converted to relative units before analysis. In univariate analysis, EVC antibodies were significantly associated with the risk of MI in men (P=0.009) but not in women. Men with MI had a significantly higher mean level of EVC antibodies than matched controls (P=0.014). High antibody levels to EVC were associated with an increased risk of MI in men aged 25 to 49 years (relative risk [RR] 4.34, P<0.001) but not in older men (>50 years of age). Women with MI also showed a trend toward higher antibody levels than control women, but the difference was not statistically significant. Antibody levels to whole CBV-5 or adenovirus hexon protein appeared to be no different among case patients versus control subjects. CONCLUSIONS: If we assume that a high level of EVC antibodies reflects a history of relatively frequent enterovirus infections, the present observation might suggest that enterovirus infections increase the risk of MI at least in middle-aged men. Further studies are needed to understand possible clinical significance of this observation.

Adult↗
PubMed2002

Role of non-polio enterovirus infection in pediatric hemolytic uremic syndrome.

Verocytotoxin-producing Escherichia coli(VTEC) infections cause most cases of hemolytic uremic syndrome (HUS); 10-30% of patients, however, are negative for VTEC infection. The etiology of HUS in VTEC-negative cases remains poorly understood. Before the association between VTEC infection and HUS was recognized, sporadic cases of HUS with enterovirus infection were reported in the literature. Since May 1988, most cases of HUS in Italy have been reported to the Italian surveillance system, and in 73% of these, evidence of VTEC infection was demonstrated. The aim of this study was to determine whether the frequency of enteroviral infections was different in the acute phase of VTEC-positive and VTEC-negative HUS. Eighty-nine patients were investigated for enteroviral infection, of whom 58 were VTEC positive and 31 VTEC negative. Two serum samples from each patient were examined for seroconversion to enterovirus (coxsackie, echovirus, and picornavirus) by a complement fixation test. Serological evidence of acute infection with non-polio enterovirus was found in 33 patients (37%) [20/58 (34.5%) VTEC positive and 13/31 (41.9%) VTEC negative]. There was no statistically significant difference between the two groups. These results demonstrate that there are no significant differences for enteroviral infection in VTEC-positive and VTEC-negative patients and, therefore, enteroviral infections should not be considered a cause of HUS in VTEC-negative children.

Child↗
PubMed1998

Simultaneous onset of type 1 diabetes mellitus in identical infant twins with enterovirus infection.

This report describes classical Type 1 insulin deficient diabetes mellitus (DM) arising in twins aged 14 months, both of whom had evidence of enterovirus infection. The diagnosis of Type 1 DM was made in the second twin within 12 days of the first. Enterovirus infection was detected in each twin at diagnosis by polymerase chain reaction (PCR). Both twins were negative for enterovirus by PCR 5 months following diagnosis, although both were then positive for islet cell antibodies. Sequencing of the amplicons produced by PCR suggested that the viruses from each twin were not the same but that they were both variants related to echovirus 6.

Age of Onset↗
PubMed1994

Therapeutic effects of bovine enterovirus infections on autochthonous rat ovarian carcinomas induced by 7,12-dimethylbenz (a) anthracene (DMBA).

It has been previously reported that infection by a bovine enterovirus (MZ-468), which does not infect normal human cells, was remarkably effective for the therapy of adult T cell leukemia (ATL) in experimental rabbit models (Shingu et al. 1991). Therapeutic treatment studies were performed twice on 30 and 20 autochthonous rat ovarian carcinomas induced by DMBA. The average tumor size of the virus treatment group was significantly smaller than the control group when analyzed by a nonparametric Mann-Whitney method (p < 0.06 and 0.002 for the 1st and 2nd experiments, respectively). These results indicate that an enterovirus infection may be clinically useful for the therapy of human ovarian cancers with bad prognoses.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2004

Enterovirus infections with beta-cell tropic strains are frequent in siblings of children diagnosed with type 1 diabetes children and in association with elevated levels of GAD65 antibodies.

Enterovirus infections have been associated with type 1 diabetes in a number of reports. Recent prospective studies have suggested that enterovirus infections initiate the autoimmune process. Variation in virulence and replication pattern between strains of a serotype has also been shown. The aim was to study if there were specific Coxsackievirus strains that were associated more often with the type 1 diabetes children than with controls and/or siblings and to analyse if there was any time-relationship between such infections and the appearance of antibodies against glutamic acid decarboxylase 65 (GAD65). In the present study, serum was tested from newly diagnosed type 1 diabetes children, their siblings and matched controls for neutralising antibodies against different strains of Coxsackievirus B (CBV). Tests for the presence of antibodies against GAD65 in the same groups were also carried out. Newly diagnosed type 1 diabetes children revealed higher titres of neutralising antibodies against a strain of Coxsackievirus B4 (CBV-4, VD2921) that has been shown to cause persistent infection in human pancreatic islet cells. The type 1 diabetes child and its sibling often encountered the same infection. Among the former, 16 of 27 (59%) had a significant rise in neutralising antibodies. Eight of the type 1 diabetes children had such a rise against a recombinant strain, V89 4557. Among the siblings 10 of 13 (77%) had significant titre increases. Among the type 1 diabetes children, increasing neutralising titres was associated positively with increasing antibody levels against GAD65. All siblings with antibodies against GAD 65 had significant titre increase against any of the CBV strains.

Adolescent↗