Lower PCT concentrations in children hospitalized with CAP were associated with a reduced risk of typical bacterial detection and may help identify children who would not benefit from antibiotic treatment.

We evaluated a multiplexed PCR panel for the detection of 16 bacterial, viral, and fungal pathogens in cerebrospinal fluid. Panel results were compared to routine testing, and discrepancies were resolved by additional nucleic acid amplification tests or sequencing. Overall, the positive and negative agreements across methods were 92.9% and 91.9%, respectively. A cute meningoencephalitis (ME) is an inflammatory disease of the central nervous system (CNS) that can result in significant morbidity and mortality. Prompt diagnosis is essential for optimal outcomes (1-3) and resource utilization (4), but confirming an infectious etiology is often difficult and time-consuming. Culture remains the diagnostic gold standard for the diagnosis of bacterial and fungal ME, while nucleic acid (NA) amplification using PCR is used routinely for viruses.BioFire Diagnostics (Salt Lake City, UT) has developed a fully automated, multiplexed PCR system called the FilmArray (FA) that can test for large combinations of infectious agents simultaneously. A FilmArray ME panel was designed to detect and identify 16 common bacteria, viruses, and yeasts directly from cerebrospinal fluid (CSF). The purpose of this study was to evaluate the test performance of a research only (RUO) version of the panel ( Table 1) compared to that of conventional microbiologic testing.(Portions of the this study were previously presented at the American Society for Microbiology Meeting, Boston, MA, 17 to 20 May 2014, and at the Infectious Diseases Society of America Meeting, Philadelphia, PA, 8 to 12 October 2014.) CSF samples obtained by lumbar puncture between August 2012 and March 2014 were retrieved from frozen storage (Ϫ20°C) at the University of Utah's ARUP Laboratories and Primary Children's Hospital (Salt Lake City, UT). Specimens were eligible to be included in the study if (i) they had been previously analyzed with at least one conventional method (bacterial culture, viral PCR, and/or cryptococcal antigen [CrAG]) and (ii) there was an adequate residual volume for FA ME testing and discrepancy resolution testing if necessary. Only the first CSF specimen submitted with adequate volume per patient was included in the study repository. Specimens were linked to the routine microbiology results and then deidentified prior to FA ME testing.FA ME testing was performed by investigators blinded to the conventional test results. The RUO multiplex panel was used per the manufacturer's instructions. Briefly, 200 l of CSF was diluted 1:4 with sample buffer and was injected into a single-use FA ME pouch. Testing was performed on the commercially available FA instrument with RUO software. NA extraction, purification, amplification, and results interpretations are automated within the FA system. Assay run time was approximately 1 h with 5 min of hands-on work.ARUP Laboratories-developed real-time PCR tests (LDTs) (5-9) were used to resolve specimens with viral NA detected by FA ME testing that had not been previously tested by PCR as a part of routine clinical care. ...

Background Invasive Staphylococcus aureus infections are a common cause of morbidity and mortality in children. In the early 2000's the proportion of infections due the methicillin-resistant S. aureus (MRSA) increased rapidly. We described the clinical and molecular epidemiology of invasive S. aureus disease in a pediatric population. Methods We prospectively identified children in Utah with invasive S. aureus infections. Medical records were reviewed to determine diagnosis and clinical characteristics. Isolates were genotyped using multi-locus sequence typing. The presence of genes encoding the Panton-Valentine leukocidin (PVL) was determined using polymerase chain reaction. Results Over a 4-year period between January 2009 and December 2012, we identified 357 children, hospitalized at Primary Children's Hospital, with invasive S. aureus infections and isolates available for the study. Methicillin-susceptible S. aureus (MSSA) caused 79% of disease, while MRSA caused only 21% of disease. Mortality associated with invasive S. aureus infection was 3.6%. The most common diagnoses were osteoarticular infections (38%) followed by central line associated blood stream infections (19%) and pneumonia (12%). We identified 41 multi-locus sequence types. The majority of isolates belonged to 6

Background Following widespread use of the Haemophilus influenzae serotype b (Hib) vaccine, H. influenzae serotype a (Hia) has emerged as an important pathogen in children in some regions. We describe the clinical features and molecular epidemiology of invasive Hia disease in children in Utah over an 11-year period. Methods We identified cases of invasive Hia disease, defined as detection of Hia from a normally sterile site, in children aged <18 years from Utah between 2007 and 2017. Medical records were reviewed to determine demographic characteristics and clinical outcomes. Available Hia isolates were genotyped using multilocus sequence typing, and phylogenetic division was determined using sodC polymerase chain reaction. Presence of the putative virulence-associated IS1016-bexA duplication-deletion was evaluated. Results We identified 51 children with invasive Hia. The average annual incidence was 1.7 cases per 100 000 children aged <5 years; 4.8 cases per 100 000 children aged <1 year. The median age was 11.3 months. The most common clinical presentation was meningitis (53%), followed by pneumonia (14%) and septic arthritis (14%). Twenty-two children (43%) required admission to an intensive care unit; 1 died. Sequence type (ST) 62, phylogenetic division II isolates caused 75% (21/28) of disease. No isolates contained the virulence-associated IS1016-bexA duplication-deletion. Conclusions Hia is a significant cause of severe invasive bacterial infection in Utah. The majority of infections were caused by ST62 isolates, a phylogenetic division II Hia type that lacks the IS1016-bexA duplication-deletion. Hia ST62 has not been commonly reported elsewhere, suggesting a unique molecular epidemiology in our population.

BackgroundFollowing widespread use of the Haemophilus influenzaeserotype b (Hib) vaccine,H. influenzae serotype a (Hia) has emerged as an important pathogen in children. Rates of Hia disease are particularly high in Utah. We describe the clinical features and molecular epidemiology of invasive Hia disease in children in Utah over 11 years.MethodsCases of invasive Hia disease in children less than 18 years were identified through electronic clinical and microbiology records. Demographic data and clinical outcomes were abstracted from the medical record for all cases. Available Hia isolates were collected for molecular analysis. Isolates were genotyped by multi-locus sequence typing (MLST) and clonal division was determined using sodC PCR. Presence or absence of the putative virulence-associated IS1016-bexA duplication-deletion was evaluated.ResultsWe identified 51 children with invasive Hia between 2007 and 2017. Median age was 11.3 months. The average annual incidence was 1.7 cases per 100,000 children aged <5 years (95% CI 1.2–2.2). Incidence was highest among children less than one year of age (4.8/100,000; 95% CI 3.1–6.9). Incidence rates were similar by race and ethnicity, although the confidence intervals were wide. The annual number of cases was similar over the 11-year study period (figure). The most common clinical manifestation was meningitis (54%; half had intracranial complications, 25% suffered hearing loss), followed by pneumonia (14%), and arthritis (14%). Twenty-two children (44%) required ICU care and one child died. Twenty-eight isolates (56%) were available for molecular analysis. ST62, clonal division II isolates caused 75% (21/28) of disease. No isolates contained the virulence-associated IS1016-bexA duplication-deletion.ConclusionHia is an important cause of severe invasive bacterial infection in Utah. Molecular analyses revealed that a majority of infections were caused by ST62 isolates, a clonal division II Hia type lacking the IS1016-bexA duplication-deletion. Hia ST62 has not been commonly reported in other settings, suggesting a unique molecular epidemiology in our population. Disclosures All authors: No reported disclosures.