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Dive into the research topics where Billie A. Juni is active.

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Featured researches published by Billie A. Juni.


The Journal of Infectious Diseases | 2010

Increased Penicillin Nonsusceptibility of Nonvaccine-Serotype Invasive Pneumococci Other than Serotypes 19A and 6A in Post-7-Valent Conjugate Vaccine Era

Robert E. Gertz; Zhongya Li; Fabiana Cristina Pimenta; Delois Jackson; Billie A. Juni; Ruth Lynfield; James H. Jorgensen; Maria da Gloria Carvalho; Bernard Beall

According to population-based invasive pneumococcal surveillance in the United States during 2007, 898 (26%) of 3,511 isolates were penicillin nonsusceptible. Non-7-valent pneumococcal conjugate vaccine (PCV7) serotypes other than 19A accounted for 40% of these penicillin-nonsusceptible isolates; of these, serotypes 15A (11%), 23A (8%), 35B (8%), and 6C (5%) were most common (cumulatively 32% of penicillin-nonsusceptible isolates). Each except 6C represented a single serotype and clonal complex combination that predated the introduction of PCV7. We evaluated the genetic characteristics and nonsusceptibility to penicillin of non- PCV7 serotypes, and we found increased proportions of specific penicillin-nonsusceptible clones in serotypes 15A, 23A, 35B, and 6C, which potentially indicates a basic change of population structure within these individual serotypes.


The New England Journal of Medicine | 2009

Emergence of ciprofloxacin-resistant Neisseria meningitidis in North America.

Henry M. Wu; Brian H. Harcourt; Cynthia Hatcher; Stanley C. Wei; Ryan T. Novak; Xin Wang; Billie A. Juni; Anita Glennen; David Boxrud; Jean Rainbow; Susanna Schmink; Raydel Mair; M. Jordan Theodore; Molly A. Sander; Tracy K. Miller; Kirby Kruger; Amanda C. Cohn; Thomas A. Clark; Nancy E. Messonnier; Leonard W. Mayer; Ruth Lynfield

We report on three cases of meningococcal disease caused by ciprofloxacin-resistant Neisseria meningitidis, one in North Dakota and two in Minnesota. The cases were caused by the same serogroup B strain. To assess local carriage of resistant N. meningitidis, we conducted a pharyngeal-carriage survey and isolated the resistant strain from one asymptomatic carrier. Sequencing of the gene encoding subunit A of DNA gyrase (gyrA) revealed a mutation associated with fluoroquinolone resistance and suggests that the resistance was acquired by means of horizontal gene transfer with the commensal N. lactamica. In susceptibility testing of invasive N. meningitidis isolates from the Active Bacterial Core surveillance system between January 2007 and January 2008, an additional ciprofloxacin-resistant isolate was found, in this case from California. Ciprofloxacin-resistant N. meningitidis has emerged in North America.


Pediatrics | 2005

Outbreak of Osteomyelitis/Septic Arthritis Caused by Kingella kingae Among Child Care Center Attendees

Karen M. Kiang; Folashade Ogunmodede; Billie A. Juni; David Boxrud; Anita Glennen; Joanne M. Bartkus; Elizabeth Cebelinski; Kathleen Harriman; Steven Koop; Ralph Faville; Richard N. Danila; Ruth Lynfield

Objective.Kingella kingae often colonizes the oropharyngeal and respiratory tracts of children but infrequently causes invasive disease. In mid-October 2003, 2 confirmed and 1 probable case of K kingae osteomyelitis/septic arthritis occurred among children in the same 16- to 24-month-old toddler classroom of a child care center. The objective of this study was to investigate the epidemiology of K kingae colonization and invasive disease among child care attendees. Methods.Staff at the center were interviewed, and a site visit was performed. Oropharyngeal cultures were obtained from the staff and children aged 0 to 5 years to assess the prevalence of Kingella colonization. Bacterial isolates were subtyped by pulsed-field gel electrophoresis (PFGE), and DNA sequencing of the 16S rRNA gene was performed. A telephone survey inquiring about potential risk factors and the general health of each child was also conducted. All children and staff in the affected toddler classroom were given rifampin prophylaxis and recultured 10 to 14 days later. For epidemiologic and microbiologic comparison, oropharyngeal cultures were obtained from a cohort of children at a control child care center with similar demographics and were analyzed using the same laboratory methods. The main outcome measures were prevalence and risk factors for colonization and invasive disease and comparison of bacterial isolates by molecular subtyping and DNA sequencing. Results.The 2 confirmed case patients required hospitalization, surgical debridement, and intravenous antibiotic therapy. The probable case patient was initially misdiagnosed; MRI 16 days later revealed evidence of ankle osteomyelitis. The site visit revealed no obvious outbreak source. Of 122 children in the center, 115 (94%) were cultured. Fifteen (13%) were colonized with K kingae, with the highest prevalence in the affected toddler classroom (9 [45%] of 20 children; all case patients tested negative but had received antibiotics). Six colonized children were distributed among the older classrooms; 2 were siblings of colonized toddlers. No staff (n = 28) or children aged <16 months were colonized. Isolates from the 2 confirmed case patients and from the colonized children had an indistinguishable PFGE pattern. No risk factors for invasive disease or colonization were identified from the telephone survey. Of the 9 colonized toddlers who took rifampin, 3 (33%) remained positive on reculture; an additional toddler, initially negative, was positive on reculture. The children of the control child care center demonstrated a similar degree and distribution of K kingae colonization; of 118 potential subjects, 45 (38%) underwent oropharyngeal culture, and 7 (16%) were colonized with K kingae. The highest prevalence again occurred in the toddler classrooms. All 7 isolates from the control facility had an indistinguishable PFGE pattern; this pattern differed from the PFGE pattern observed from the outbreak center isolates. 16S rRNA gene sequencing demonstrated that the outbreak K kingae strain exhibited >98% homology to the ATCC-type strain, although several sequence deviations were present. Sequencing of the control center strain demonstrated more homology to the outbreak center strain than to the ATCC-type strain. Conclusions.This is the first reported outbreak of invasive K kingae disease. The high prevalence in the affected toddler class and the matching PFGE pattern are consistent with child-to-child transmission within the child care center. Rifampin was modestly effective in eliminating carriage. DNA sequence analysis suggests that there may be considerable variability within the species K kingae and that different K kingae strains may demonstrate varying degrees of pathogenicity.


Infectious Diseases in Obstetrics & Gynecology | 2008

Antibiotic Resistance Patterns in Invasive Group B Streptococcal Isolates

Mei Lin Castor; Cynthia G. Whitney; Kathryn Como-Sabetti; Richard R. Facklam; Patricia Ferrieri; Joanne M. Bartkus; Billie A. Juni; Paul R. Cieslak; Monica M. Farley; Nellie B. Dumas; Stephanie J. Schrag; Ruth Lynfield

Antibiotics are used for both group B streptococcal (GBS) prevention and treatment. Active population-based surveillance for invasive GBS disease was conducted in four states during 1996–2003. Of 3813 case-isolates, 91.0% (3471) were serotyped, 77.1% (2937) had susceptibility testing, and 46.6% (3471) had both. All were sensitive to penicillin, ampicillin, cefazolin, cefotaxime, and vancomycin. Clindamycin and erythromycin resistance was 12.7% and 25.6%, respectively, and associated with serotype V (P < .001). Clindamycin resistance increased from 10.5% to 15.0% (X 2 for trend 12.70; P < .001); inducible clindamycin resistance was associated with the erm genotype. Erythromycin resistance increased from 15.8% to 32.8% (X 2 for trend 55.46; P < .001). While GBS remains susceptible to beta-lactams, resistance to alternative agents such as erythromycin and clindamycin is an increasing concern.


Pediatric Infectious Disease Journal | 2011

Risk factors for household transmission of community-associated methicillin-resistant Staphylococcus aureus.

Jessica Nerby; Rachel J. Gorwitz; Lindsey Lesher; Billie A. Juni; Selina Jawahir; Ruth Lynfield; Kathleen Harriman

Background: Methicillin-resistant Staphylococcus aureus (MRSA) has emerged as a community pathogen. Community-associated (CA) MRSA infections have occurred among multiple members of a household. We describe the incidence of and risk factors for MRSA colonization among household contacts of children with CA-MRSA infections. Methods: MRSA-infected children <18 years of age who lacked established healthcare-associated MRSA risk factors were identified through surveillance at 12 Minnesota hospital laboratories. Nasal swab specimens and information on medical history and hygiene behaviors were collected from case-patients and enrolled household contacts during home visits. S. aureus isolates obtained from nasal cultures were screened for oxacillin resistance. Results: In all, 236 households consisting of 236 case-patients and 712 household contacts were enrolled. Home visits were conducted on an average of 69 days after the onset of symptom in case-patients (range: 16–178 days). Twenty-nine (13%) case-patients and 82 (12%) household contacts had MRSA nasal colonization. Nasal MRSA colonization in ≥1 household contact occurred in 58 (25%) households. Household contacts who assisted the case-patient to bathe or who shared balms/ointments/lotion with the case-patient were more likely to be colonized (P < 0.01, P < 0.05), whereas those who reported using antibacterial versus nonantibacterial soap for hand washing were less likely to be colonized (P < 0.05) with MRSA clonally related to the case-patient infection isolate. Conclusions: Only 13% of case-patients had MRSA nasal colonization on an average of 69 days after their initial MRSA infection. CA-MRSA colonization may be short-lived or may occur at non-nasal sites. One quarter of households had at least one household contact colonized with MRSA. Modifiable behaviors, such as sharing personal items, may contribute to transmission.


The Journal of Infectious Diseases | 2005

An Outbreak of Pontiac Fever with Respiratory Distress among Workers Performing High-Pressure Cleaning at a Sugar-Beet Processing Plant

Mei Lin Castor; Elizabeth A. Wagstrom; Richard N. Danila; Kirk E. Smith; Timothy S. Naimi; John M. Besser; Keith Peacock; Billie A. Juni; John M. Hunt; Joanne M. Bartkus; Steven R. Kirkhorn; Ruth Lynfield

BACKGROUND In August 2000, the Minnesota Department of Health was notified of and investigated an outbreak of febrile respiratory illness among workers at a sugar-beet processing plant. METHODS A case was defined as fever and respiratory symptoms occurring in a worker at the sugar-beet plant on or after 31 July 2000. Case patients were interviewed, medical and work records were reviewed, and clinical samples were obtained. The plant was inspected, and environmental samples were collected. RESULTS Fourteen of 15 case patients performed high-pressure water cleaning in the confined space of an evaporator vessel. Symptoms included fever and chills (100%), chest tightness (93%), cough (80%), and shortness of breath (73%). In case patients, median temperature was 39.4 degrees C, median oxygen saturation was 93%, and median white blood cell count was 12x10(3) cells/ mu L. Four (29%) of 14 case patients showed evidence of Legionella pneumophila exposure, according to serologic testing. Water sources contained up to 10(5) cfu/mL of L. pneumophila and 22,200 endotoxin units/mL. CONCLUSIONS Outbreak features were consistent with Pontiac fever. Respiratory symptoms, which are atypical for Pontiac fever, could be attributed to a high exposure dose of L. pneumophila from confined-space aerosolization or to endotoxin exposure. This outbreak demonstrates the potential occupational hazards for those performing high-pressure cleaning in confined spaces.


Journal of Clinical Microbiology | 2012

Evaluation of New Biomarker Genes for Differentiating Haemophilus influenzae from Haemophilus haemolyticus

M. Jordan Theodore; Raydel Anderson; Xin Wang; Lee S. Katz; Jeni T. Vuong; Melissa E. Bell; Billie A. Juni; Sara A. Lowther; Ruth Lynfield; Jessica R. MacNeil; Leonard W. Mayer

ABSTRACT PCR detecting the protein D (hpd) and fuculose kinase (fucK) genes showed high sensitivity and specificity for identifying Haemophilus influenzae and differentiating it from H. haemolyticus. Phylogenetic analysis using the 16S rRNA gene demonstrated two distinct groups for H. influenzae and H. haemolyticus.


The Journal of Infectious Diseases | 2013

Geographic and Temporal Trends in Antimicrobial Nonsusceptibility in Streptococcus pneumoniae in the Post-vaccine era in the United States

Ruth Link-Gelles; Ann Thomas; Ruth Lynfield; Sue Petit; William Schaffner; Lee H. Harrison; Monica M. Farley; Deborah Aragon; Megin Nicols; Pam Daily Kirley; Shelley M. Zansky; James H. Jorgensen; Billie A. Juni; Delois Jackson; Matthew R. Moore; Marc Lipsitch

BACKGROUND We examined whether observed increases in antibiotic nonsusceptible nonvaccine serotypes after introduction of pneumococcal conjugate vaccine in the United States in 2000 were driven primarily by vaccine or antibiotic use. METHODS  Using active surveillance data, we evaluated geographic and temporal differences in serotype distribution and within-serotype differences during 2000-2009. We compared nonsusceptibility to penicillin and erythromycin by geography after standardizing differences across time, place, and serotype by regressing standardized versus crude proportions. A regression slope (RS) approaching zero indicates greater importance of the standardizing factor. RESULTS  Through 2000-2006, geographic differences in nonsusceptibility were better explained by within-serotype prevalence of nonsusceptibility (RS 0.32, 95% confidence interval [CI], .08-.55 for penicillin) than by geographic differences in serotype distribution (RS 0.71, 95% CI, .44-.97). From 2007-2009, serotype distribution differences became more important for penicillin (within-serotype RS 0.52, 95% CI, .11-.93; serotype distribution RS 0.57, 95% CI, .14-1.0). CONCLUSIONS  Differential nonsusceptibility, within individual serotypes, accounts for most geographic variation in nonsusceptibility, suggesting selective pressure from antibiotic use, rather than differences in serotype distribution, mainly determines nonsusceptibility patterns. Recent trends suggest geographic differences in serotype distribution may be affecting the prevalence of nonsusceptibility, possibly due to decreases in the number of nonsusceptible serotypes.


Pediatric Infectious Disease Journal | 2013

Invasive pneumococcal disease among children with and without sickle cell disease in the United States, 1998 to 2009

Amanda B. Payne; Ruth Link-Gelles; Ijeoma Azonobi; W. Craig Hooper; Bernard Beall; James H. Jorgensen; Billie A. Juni; Matthew R. Moore

Background: Children with sickle cell disease (SCD) are at increased risk of illness and death from invasive pneumococcal disease (IPD). The introduction in 2000 of the 7-valent pneumococcal conjugate vaccine and penicillin prophylaxis for children with SCD has greatly reduced the incidence of IPD in this population. However, a recent report suggested an increase in cases of IPD in children with SCD. Methods: Using data from Active Bacterial Core surveillance, we analyzed trends in hospitalizations, mortality and serotype among children with SCD compared with other children. We used neonatal screening data to estimate SCD population denominators for each Active Bacterial Core surveillance site. Results: From 1998 to 2009, 3069 cases of IPD occurred among African-American children less than 18 years of age in the Active Bacterial Core surveillance catchment area. Of these, 127 (4.1%) had SCD identified by medical chart review and 185 (6.0%) had 1 or more IPD risk factors, excluding SCD. Rates of IPD among children with SCD declined by 53% (1118 vs. 530 per 100,000) whereas the overall rates among African-American children declined by 74% (54 to 14 per 100,000). For all time periods, children with SCD and IPD were more likely to be hospitalized (84%–92% vs. 31%–56%) and more likely to die (6%–17% vs. 1%–2%) than children with no risk factors. Conclusions: Although the rate of IPD in children with SCD has dropped dramatically since 7-valent pneumococcal conjugate vaccine introduction, the rate of IPD in children with SCD remains higher than that of the general population of African-American children, pointing to the need for more effective prevention efforts to prevent IPD in children with SCD.


Emerging Infectious Diseases | 2014

Lethal Factor and Anti-Protective Antigen IgG Levels Associated with Inhalation Anthrax, Minnesota, USA

Mark D. Sprenkle; Jayne Griffith; William Marinelli; Anne E. Boyer; Conrad P. Quinn; Nicki T. Pesik; Alex R. Hoffmaster; Joseph Keenan; Billie A. Juni; David D. Blaney

Bacillus anthracis was identified in a 61-year-old man hospitalized in Minnesota, USA. Cooperation between the hospital and the state health agency enhanced prompt identification of the pathogen. Treatment comprising antimicrobial drugs, anthrax immune globulin, and pleural drainage led to full recovery; however, the role of passive immunization in anthrax treatment requires further evaluation.

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Ruth Lynfield

Centers for Disease Control and Prevention

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Anita Glennen

Centers for Disease Control and Prevention

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Kathleen Harriman

California Department of Public Health

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Bernard Beall

National Center for Immunization and Respiratory Diseases

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James H. Jorgensen

University of Texas Health Science Center at San Antonio

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Matthew R. Moore

Centers for Disease Control and Prevention

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David Boxrud

Public health laboratory

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Ann Thomas

Brigham and Women's Hospital

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