Carol Glaser

California Department of Public Health, Richmond, California, United States

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Publications (111)838.32 Total impact

  • Genome Medicine 12/2015; 7(1). DOI:10.1186/s13073-015-0235-2 · 5.34 Impact Factor
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    ABSTRACT: Since Middle East respiratory syndrome coronavirus (MERS-CoV) first emerged, the California Department of Public Health has coordinated efforts to identify possible cases in travelers to California, USA, from affected areas. During 2013-2014, the department investigated 54 travelers for MERS-CoV; none tested positive, but 32 (62%) of 52 travelers with suspected MERS-CoV had other respiratory viruses.
    Emerging infectious diseases 09/2015; 21(9). DOI:10.3201/eid2109.150476 · 6.75 Impact Factor
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    Karen C Bloch · Carol A Glaser ·
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    ABSTRACT: Encephalitis is a devastating illness that commonly causes neurologic disability and has a case fatality rate >5% in the United States. An etiologic agent is identified in <50% of cases, making diagnosis challenging. The Centers for Disease Control and Prevention Emerging Infections Program (EIP) Encephalitis Project established syndromic surveillance for encephalitis in New York, California, and Tennessee, with the primary goal of increased identification of causative agents and secondary goals of improvements in treatment and outcome. The project represents the largest cohort of patients with encephalitis studied to date and has influenced case definition and diagnostic evaluation of this condition. Results of this project have provided insight into well-established causal pathogens and identified newer causes of infectious and autoimmune encephalitis. The recognition of a possible relationship between enterovirus D68 and acute flaccid paralysis with myelitis underscores the need for ongoing vigilance for emerging causes of neurologic disease.
    Emerging Infectious Diseases 09/2015; 21(9). DOI:10.3201/eid2109.150295 · 6.75 Impact Factor
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    ABSTRACT: To evaluate factors during acute presumed childhood encephalitis that are associated with development of long-term neurological sequelae. A total of 217 patients from Rady Children's Hospital San Diego with suspected encephalitis who met criteria for the California Encephalitis Project were identified. A cohort of 99 patients (40 females, 59 males, age 2 months-17 years) without preexisting neurological conditions, including prior seizures or abnormal brain magnetic resonance imaging scans was studied. Mean duration of follow-up was 29 months. Factors that had a relationship with the development of neurological sequelae (defined as developmental delay, learning difficulties, behavioral problems, or focal neurological findings) after acute encephalitis were identified. Neurological sequelae at follow-up was associated with younger age (6.56 versus 9.22 years) at presentation (P = 0.04) as well as an initial presenting sign of seizure (P = 0.03). Duration of hospital stay (median of 7 versus 15.5 days; P = 0.02) was associated with neurological sequelae. Of the patients with neurological sequelae, a longer hospital stay was associated with patients of an older age (P = 0.04). Abnormalities on neuroimaging (P = 1.00) or spinal fluid analysis (P = 1.00) were not uniquely associated with neurological sequelae. Children who were readmitted after their acute illness (P = 0.04) were more likely to develop neurological sequelae. There was a strong relationship between the patients who later developed epilepsy and those who developed neurological sequelae (P = 0.02). Limited data are available on the long-term neurological outcomes of childhood encephalitis. Almost half of our patients were found to have neurological sequelae at follow-up, indicating the importance of earlier therapies to improve neurological outcome. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 06/2015; 53(3). DOI:10.1016/j.pediatrneurol.2015.05.017 · 1.70 Impact Factor
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    Clinical Infectious Diseases 04/2015; 61(2). DOI:10.1093/cid/civ314 · 8.89 Impact Factor
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    ABSTRACT: Enterovirus D68 was implicated in a widespread outbreak of severe respiratory illness across the USA in 2014 and has also been reported sporadically in patients with acute flaccid myelitis. We aimed to investigate the association between enterovirus D68 infection and acute flaccid myelitis during the 2014 enterovirus D68 respiratory outbreak in the USA. Patients with acute flaccid myelitis who presented to two hospitals in Colorado and California, USA, between Nov 24, 2013, and Oct 11, 2014, were included in the study. Additional cases identified from Jan 1, 2012, to Oct 4, 2014, via statewide surveillance were provided by the California Department of Public Health. We investigated the cause of these cases by metagenomic next-generation sequencing, viral genome recovery, and enterovirus D68 phylogenetic analysis. We compared patients with acute flaccid myelitis who were positive for enterovirus D68 with those with acute flaccid myelitis but negative for enterovirus D68 using the two-tailed Fisher's exact test, two-sample unpaired t test, and Mann-Whitney U test. 48 patients were included: 25 with acute flaccid myelitis, two with enterovirus-associated encephalitis, five with enterovirus-D68-associated upper respiratory illness, and 16 with aseptic meningitis or encephalitis who tested positive for enterovirus. Enterovirus D68 was detected in respiratory secretions from seven (64%) of 11 patients comprising two temporally and geographically linked acute flaccid myelitis clusters at the height of the 2014 outbreak, and from 12 (48%) of 25 patients with acute flaccid myelitis overall. Phylogenetic analysis revealed that all enterovirus D68 sequences associated with acute flaccid myelitis grouped into a clade B1 strain that emerged in 2010. Of six coding polymorphisms in the clade B1 enterovirus D68 polyprotein, five were present in neuropathogenic poliovirus or enterovirus D70, or both. One child with acute flaccid myelitis and a sibling with only upper respiratory illness were both infected by identical enterovirus D68 strains. Enterovirus D68 viraemia was identified in a child experiencing acute neurological progression of his paralytic illness. Deep metagenomic sequencing of cerebrospinal fluid from 14 patients with acute flaccid myelitis did not reveal evidence of an alternative infectious cause to enterovirus D68. These findings strengthen the putative association between enterovirus D68 and acute flaccid myelitis and the contention that acute flaccid myelitis is a rare yet severe clinical manifestation of enterovirus D68 infection in susceptible hosts. National Institutes of Health, University of California, Abbott Laboratories, and the Centers for Disease Control and Prevention. Copyright © 2015 Elsevier Ltd. All rights reserved.
    The Lancet Infectious Diseases 03/2015; 15(6). DOI:10.1016/S1473-3099(15)70093-9 · 22.43 Impact Factor
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    ABSTRACT: To evaluate factors associated with the development of epilepsy after resolution of presumed childhood encephalitis. A total of 217 patients with suspected encephalitis who met criteria for the California Encephalitis Project were identified. Evaluable outcome information was available for 99 patients (40 girls, 59 boys, ages 2 months to 17 years) without preexisting neurological conditions, including prior seizures or abnormal brain magnetic resonance imaging scans. We identified factors correlated with the development of epilepsy after resolution of the acute illness. Development of epilepsy was correlated with the initial presenting sign of seizure (P < 0.001). With each additional antiepileptic drug used to control seizures, the odds ratio of developing epilepsy was increased twofold (P < 0.001). An abnormal electroencephalograph (P < 0.05) and longer hospital duration (median of 8 versus 21 days) also correlated with development of epilepsy (P < 0.01). The need for medically induced coma was associated with epilepsy (P < 0.001). Seizures in those patients were particularly refractory, often requiring longer than 24 hours to obtain seizure control. Individuals who required antiepileptic drugs at discharge (P < 0.001) or were readmitted after their acute illness (P < 0.001) were more likely to develop epilepsy. Of our patients who were able to wean antiepileptic drugs after being started during hospitalization, 42% were successfully tapered off within 6 months. Limited data are available on the risk of developing epilepsy after childhood encephalitis. This is the first study that not only identifies risk factors for the development of epilepsy, but also provides data regarding the success rate of discontinuing antiepileptic medication after resolution of encephalitis. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 03/2015; 53(1). DOI:10.1016/j.pediatrneurol.2015.03.016 · 1.70 Impact Factor
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    ABSTRACT: Diagnosing pediatric encephalitis is challenging because of varied clinical presentation, nonspecific neuroimaging features, and rare confirmation of causality. We reviewed acute neuroimaging of children with clinically suspected encephalitis to identify findings that may correlate with etiology and length of stay. Imaging of 141 children with clinically suspected encephalitis as part of The California Encephalitis Project from 2005 to 2012 at a single institution was reviewed to compare the extent of neuroimaging abnormalities to patient age, gender, length of stay, and unknown, possible, or confirmed pathogen. Scan review was blinded and categorized by extent and distribution of abnormal findings. Abnormal findings were evident on 23% (22/94) of computed tomography and 50% (67/134) of magnetic resonance imaging studies in the acute setting. Twenty children with normal admission computed tomography had abnormal findings on magnetic resonance imaging performed within 2 days. Length of stay was significantly longer among children with abnormal acute magnetic resonance imaging (P < 0.001) and correlated with increased complexity (Spearman rho = 0.4, P < 0.001) categorized as: no imaging abnormality, meningeal enhancement and/or focal nonenhancing lesion, multifocal lesions, confluent lesions, and lesions plus diffusion restriction, hemorrhage, or hydrocephalus. There was no correlation between neuroimaging findings and an identifiable pathogen (P = 0.8). Abnormal magnetic resonance imaging findings are more common than abnormal computed tomography findings in pediatric encephalitis. Increasing complexity of magnetic resonance imaging findings correlated with disease severity as evidenced by longer length of stay, but were not specific for an identifiable pathogen using a standardized diagnostic encephalitis panel. Copyright © 2015 Elsevier Inc. All rights reserved.
    Pediatric Neurology 02/2015; 52(6). DOI:10.1016/j.pediatrneurol.2015.02.024 · 1.70 Impact Factor
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    ABSTRACT: Background: We describe the spectrum of etiologies associated with temporal lobe (TL) encephalitis and identify clinical and radiologic features that distinguish herpes simplex encephalitis (HSE) from its mimics. Methods: We reviewed all adult cases of encephalitis with TL abnormalities on magnetic resonance imaging (MRI) from the California Encephalitis Project. We evaluated the association between specific clinical and MRI characteristics and HSE compared with other causes of TL encephalitis and used multivariate logistic modeling to identify radiologic predictors of HSE. Results: Of 251 cases of TL encephalitis, 43% had an infectious etiology compared with 16% with a noninfectious etiology. Of infectious etiologies, herpes simplex virus was the most commonly identified agent (n = 60), followed by tuberculosis (n = 8) and varicella zoster virus (n = 7). Of noninfectious etiologies, more than half (n = 21) were due to autoimmune disease. Patients with HSE were older (56.8 vs 50.2 years; P = .012), more likely to be white (53% vs 35%; P = .013), more likely to present acutely (88% vs 64%; P = .001) and with a fever (80% vs 49%; P < .001), and less likely to present with a rash (2% vs 15%; P = .010). In a multivariate model, bilateral TL involvement (odds ratio [OR], 0.38; 95% confidence interval [CI], .18-.79; P = .010) and lesions outside the TL, insula, or cingulate (OR, 0.37; 95% CI, .18-.74; P = .005) were associated with lower odds of HSE. Conclusions: In addition to HSE, other infectious and noninfectious etiologies should be considered in the differential diagnosis for TL encephalitis, depending on the presentation. Specific clinical and imaging features may aid in distinguishing HSE from non-HSE causes of TL encephalitis.
    Clinical Infectious Diseases 01/2015; 60(9). DOI:10.1093/cid/civ051 · 8.89 Impact Factor
  • Kathleen Winter · Carol Glaser · James Watt · Kathleen Harriman ·
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    ABSTRACT: On June 13, 2014, the California Department of Public Health (CDPH) declared that a pertussis epidemic was occurring in the state when reported incidence was more than five times greater than baseline levels. The incidence of pertussis in the United States is cyclical, with peaks every 3-5 years, as the number of susceptible persons in the population increases. The last pertussis epidemic in California occurred in 2010, when approximately 9,000 cases were reported, including 808 hospitalizations and 10 infant deaths, for a statewide incidence of 24.6 cases per 100,000 population. During January 1-November 26, 2014, a total of 9,935 cases of pertussis with onset in 2014 were reported to CDPH, for a statewide incidence of 26.0 cases per 100,000. CDPH is working closely with local health departments to prioritize public health activities, with the primary goal of preventing severe cases of pertussis, which typically occurs in infants. All prenatal care providers are being encouraged to provide tetanus, diphtheria, and acellular pertussis vaccine (Tdap) to pregnant women during each pregnancy, ideally at 27-36 weeks' gestation, as is recommended by the Advisory Committee on Immunization Practices (ACIP), or refer patients to an alternative provider, such as a pharmacy or local public health department, to receive Tdap.
    MMWR. Morbidity and mortality weekly report 12/2014; 63(48):1129-32.
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    ABSTRACT: In August 2012, the California Department of Public Health (CDPH) was contacted by a San Francisco Bay area clinician who requested poliovirus testing for an unvaccinated man aged 29 years with acute flaccid paralysis (AFP) associated with anterior myelitis (i.e., evidence of inflammation of the spinal cord involving the grey matter including anterior horn cell bodies) and no history of international travel during the month before symptom onset. Within 2 weeks, CDPH had received reports of two additional cases of AFP with anterior myelitis of unknown etiology. Testing at CDPH's Viral and Rickettsial Disease Laboratory for stool, nasopharyngeal swab, and cerebrospinal fluid (CSF) did not detect the presence of an enterovirus (EV), the genus of the family Picornaviridae that includes poliovirus. Additional laboratory testing for infectious diseases conducted at the CDPH Viral and Rickettsial Disease Laboratory did not identify a causative agent to explain the observed clinical syndrome reported among the patients. To identify other cases of AFP with anterior myelitis and elucidate possible common etiologies, CDPH posted alerts in official communications for California local health departments during December 2012, July 2013, and February 2014. Reports of cases of neurologic illness received by CDPH were investigated throughout this period, and clinicians were encouraged to submit clinical samples for testing. A total of 23 cases of AFP with anterior myelitis of unknown etiology were identified. Epidemiologic and laboratory investigation did not identify poliovirus infection as a possible cause for the observed cases. No common etiology was identified to explain the reported cases, although EV-D68 was identified in upper respiratory tract specimens of two patients. EV infection, including poliovirus infection, should be considered in the differential diagnosis in cases of AFP with anterior myelitis and testing performed per CDC guidelines.
    MMWR. Morbidity and mortality weekly report 10/2014; 63(40):903-906.
  • Felicia C Chow · Carol A Glaser ·
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    ABSTRACT: The list of emerging and reemerging pathogens that cause neurologic disease is expanding. Various factors, including population growth and a rise in international travel, have contributed to the spread of pathogens to previously nonendemic regions. Recent advances in diagnostic methods have led to the identification of novel pathogens responsible for infections of the central nervous system. Furthermore, new issues have arisen surrounding established infections, particularly in an increasingly immunocompromised population due to advances in the treatment of rheumatologic disease and in transplant medicine.
    10/2014; 4(4):173-84. DOI:10.1177/1941874414540685
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    ABSTRACT: Twenty-one children with confirmed herpes simplex encephalitis were identified in the California Encephalitis Project. Noteworthy features included six (29%) patients with an initial negative herpes simplex virus CSF PCR test and 13 (59%) patients with extra-temporal lobe involvement identified by neuroimaging. Eleven cases were <4 years of age, but all four fatal cases occurred in adolescents.
    The Pediatric Infectious Disease Journal 06/2014; 33(12). DOI:10.1097/INF.0000000000000422 · 2.72 Impact Factor
  • Arun Venkatesan · Carol Ann Glaser ·

    Clinical Infectious Diseases 02/2014; 58(10). DOI:10.1093/cid/ciu124 · 8.89 Impact Factor
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    ABSTRACT: The California Department of Public Health (CDPH) conducts surveillance on severe influenza illness among California residents aged <65 years. Severe cases are defined as those resulting in admission to an intensive care unit (ICU) or death; reporting of ICU cases is voluntary, and reporting of fatal cases is mandatory. This report describes the epidemiologic, laboratory, and clinical characteristics of ICU and fatal influenza cases with symptom onset on or after September 29, 2013, and reported by January 18, 2014 of the 2013-14 influenza season. At the time of this report, local health jurisdictions (LHJs) in California had reported 94 deaths and 311 ICU admissions of patients with a positive influenza test result. The 405 reports of severe cases (i.e., fatal and ICU cases combined) were more than in any season since the 2009 pandemic caused by the influenza A (H1N1)pdm09 (pH1N1) virus. The pH1N1 virus is the predominant circulating influenza virus this season. Of 405 ICU and fatal influenza cases, 266 (66%) occurred among patients aged 41-64 years; 39 (10%) severe influenza illnesses occurred among children aged <18 years. Only six (21%) of 28 patients with fatal illness whose vaccination status was known had received 2013-14 seasonal influenza vaccine ≥2 weeks before symptom onset. Of 80 patients who died for whom sufficient information was available, 74 (93%) had underlying medical conditions known to increase the risk for severe influenza, as defined by the Advisory Committee on Immunization Practices (ACIP). Of 47 hospitalized patients with fatal illness and known symptom onset and antiviral therapy dates, only eight (17%) received neuraminidase inhibitors within 48 hours of symptom onset. This report supports previous recommendations that vaccination is important to prevent influenza virus infections that can result in ICU admission or death, particularly in high-risk populations, and that empiric antiviral treatment should be promptly initiated when influenza virus infection is suspected in hospitalized patients, despite negative results from rapid diagnostic tests.
    MMWR. Morbidity and mortality weekly report 02/2014; 63(7):143-7.
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    ABSTRACT: In five prospectively diagnosed patients with relapsing post-herpes simplex encephalitis (HSE), NMDAR-antibodies were identified. Antibody synthesis started 1-4 weeks post-HSE, preceding the neurological relapse. Three of five patients improved post-immunotherapy, one spontaneously, and one has started to improve. Two additional patients with NMDAR-antibodies, 9 with unknown neuronal surface-antibodies, and one with NMDAR and unknown antibodies were identified during retrospective assessment of 34 HSE-patients; the frequency of autoantibodies increased over time (serum p=0.004, CSF p=0.04). The three retrospectively identified NMDAR-antibody positive patients also had evidence of relapsing post-HSE. Overall, these findings indicate that HSE triggers NMDAR-antibodies and potentially other brain autoimmunity. ANN NEUROL 2013. © 2013 American Neurological Association.
    Annals of Neurology 02/2014; 75(2). DOI:10.1002/ana.24083 · 9.98 Impact Factor
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    ABSTRACT: Background. Encephalitis continues to result in substantial morbidity and mortality worldwide. Advances in diagnosis and management have been limited, in part, by a lack of consensus on case definitions, standardized diagnostic approaches, and priorities for research.Methods. In March 2012, the International Encephalitis Consortium, a committee begun in 2010 with members worldwide, held a meeting in Atlanta to discuss recent advances in encephalitis and to set priorities for future study.Results. We present a consensus document that proposes a standardized case definition and diagnostic guidelines for evaluation of adults and children with suspected encephalitis. In addition, areas of research priority, including host genetics and selected emerging infections, are discussed.Conclusions. We anticipate that this document, representing a synthesis of our discussions and supported by literature, will serve as a practical aid to clinicians evaluating patients with suspected encephalitis and will identify key areas and approaches to advance our knowledge of encephalitis. © 2013 The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: [email protected] /* */
    Clinical Infectious Diseases 10/2013; 57(8):1114-1128. DOI:10.1093/cid/cit458 · 8.89 Impact Factor
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    ABSTRACT: Background: Temporal lobe (TL) abnormalities on magnetic resonance imaging (MRI) are a common radiologic finding in encephalitis, particularly in cases of herpes simplex virus encephalitis (HSE). While bilateral TL involvement was once thought to be pathognomonic for HSE, other etiologies have been described. We examined cases with TL abnormalities on MRI from the California Encephalitis Project (CEP) to identify clinical and radiologic features that distinguish HSE from other etiologies of encephalitis. Methods: We retrospectively reviewed clinical and radiological data from adult encephalitis cases with MRI TL abnormalities from the CEP between 1998 and 2012. We excluded cases in which TL abnormalities were chronic or normal variants. χ2 or Fisher’s exact tests were used to compare categorical variables between HSE and non-HSE cases. We constructed a multivariate logistic regression model to identify radiological predictors of non-HSE etiologies in cases with TL abnormalities. Results: Of 3965 cases, 251 (6%) met criteria for TL abnormalities on MRI. 148 (59%) cases had an identified etiology; 105 were attributed to infectious agents and 60 (41%) to HSE. Other etiologies included tuberculosis (8), varicella-zoster virus (7), Balamuthia (4), enterovirus (4), Creutzfeld-Jakob (3), acute disseminated encephalomyelitis (4), neoplasm (9), paraneoplastic/autoimmune (8), vasculitis (6) and stroke (4). Among cases with an identified etiology, presenting > 1 week after symptom onset (42% vs 12%, p<0.001) and absence of fever (49% vs 20%, p=0.001) were associated with non-HSE etiologies. 71% of cases with bilateral TL involvement were due to non-HSE etiologies. Other MRI features associated with non-HSE etiologies were presence of lesions outside the TL/insula (61% vs 33%, p=0.002) and enhancement (53% vs 33%, p=0.02). In an age-adjusted multivariate logistic regression model, bilateral TL involvement (OR 0.42, 95%CI 0.18-0.95, p=0.04), abnormalities outside the TL/insula (OR 0.41, 95%CI 0.19-0.89 p=0.02) and enhancement (OR 0.41, 95%CI 0.18-0.91, p=0.03) decreased the odds of HSE. Conclusion: A substantial number of cases with TL abnormalities, including bilateral TL involvement, were not caused by HSE. Specific MRI characteristics in encephalitis cases with TL abnormalities may help distinguish HSE from other etiologies.
    IDWeek 2013 Meeting of the Infectious Diseases Society of America; 10/2013
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    ABSTRACT: Objective: To characterize the atypical cutaneous presentations in the coxsackievirus A6 (CVA6)-associated North American enterovirus outbreak of 2011-2012. Methods: We performed a retrospective case series of pediatric patients who presented with atypical cases of hand, foot, and mouth disease (HFMD) from July 2011 to June 2012 at 7 academic pediatric dermatology centers. Patients were included if they tested positive for CVA6 or if they met clinical criteria for atypical HFMD (an enanthem or exanthem characteristic of HFMD with unusual morphology or extent of cutaneous findings). We collected demographic, epidemiologic, and clinical data including history of skin conditions, morphology and extent of exanthem, systemic symptoms, and diagnostic test results. Results: Eighty patients were included in this study (median age 1.5 years, range 4 months-16 years). Seventeen patients were CVA6-positive, and 63 met clinical inclusion criteria. Ninety-nine percent of patients exhibited a vesiculobullous and erosive eruption; 61% of patients had rash involving >10% body surface area. The exanthem had a perioral, extremity, and truncal distribution in addition to involving classic HFMD areas such as palms, soles, and buttocks. In 55% of patients, the eruption was accentuated in areas of eczematous dermatitis, termed "eczema coxsackium." Other morphologies included Gianotti-Crosti-like (37%), petechial/purpuric (17%) eruptions, and delayed onychomadesis and palm and sole desquamation. There were no patients with serious systemic complications. Conclusions: The CVA6-associated enterovirus outbreak was responsible for an exanthem potentially more widespread, severe, and varied than classic HFMD that could be confused with bullous impetigo, eczema herpeticum, vasculitis, and primary immunobullous disease.
    PEDIATRICS 06/2013; 132(1). DOI:10.1542/peds.2012-3175 · 5.47 Impact Factor

  • 2013 Council of State and Territorial Epidemiologists Annual Conference; 06/2013

Publication Stats

4k Citations
838.32 Total Impact Points


  • 2008-2015
    • California Department of Public Health
      Richmond, California, United States
  • 2003-2015
    • University of California, San Francisco
      • Division of Infectious Diseases
      San Francisco, California, United States
  • 2013
    • North Shore-Long Island Jewish Health System
      New York, New York, United States
  • 2009
    • Stanford Medicine
      Stanford, California, United States
  • 2004-2008
    • California Department of Health Care Services
      Sacramento, California, United States
  • 2007
    • Children's Hospital & Research Center Oakland
      Oakland, California, United States
  • 2002
    • Centers for Disease Control and Prevention
      Атланта, Michigan, United States
  • 1999
    • Johns Hopkins University
      • Department of Medicine
      Baltimore, Maryland, United States