Effect of number of blood cultures and volume of blood on detection of bacteremia in children.

OBJECTIVE: To determine whether bacteremia can be detected more rapidly and completely by (1) obtaining two blood cultures instead of one and/or (2) collecting a larger volume of blood. STUDY DESIGN: Prospective comparison of different strategies in 300 patients undergoing blood culture for suspected bacteremia. Each patient had two samples of blood, A (2 ml) and B (9.5 ml), obtained sequentially from separate sites. The B sample was divided into three aliquots: B1 (2 ml), B2 (6 ml), and ISO (1.5 ml, quantitative culture). RESULTS: A pathogen was isolated from one or more blood cultures in 30 patients (10% of cases). When measured at 24 hours, the pathogen recovery rate for the B2 sample (72%) was higher than that for the individual small-volume samples (A = 37%, B1 = 33%; p < 0.01 for each comparison) and for the combination of the two small-volume samples (A + B1 = 47%; p = 0.04). At final (7-day) reading the pathogen recovery rate for the B2 sample (83%) was higher than that for B1 (60%; p = 0.02) and similar to the recovery rate observed with the combination of the two small-volume cultures (A + B1 = 73%; p = 0.55). CONCLUSIONS: Increasing the volume of blood inoculated into blood culture bottles improves the timely detection of bacteremia in pediatric patients and spares the patients the cost and pain of an additional venipuncture.

Utility of routine laboratory testing for detecting intra-abdominal injury in the pediatric trauma patient.

OBJECTIVE: To assess the prevalence of laboratory abnormalities (complete blood cell count, electrolytes, blood urea nitrogen, creatinine, glucose, aspartate aminotransferase, alanine aminotransferase, amylase, lipase, urinalysis [U/A]) and the sensitivity and specificity of the physical examination (PE) and screening laboratory tests for identifying intra-abdominal injury (IAI) in moderately injured pediatric patients. DESIGN, PARTICIPANTS, AND SETTING: Phase I: Retrospective chart review of 285 consecutive level II (moderately injured) trauma patients seen at a children's hospital emergency department/pediatric trauma center. All patients were received directly from the scene and had the following data recorded: mechanism of injury, Glasgow coma score, trauma score, pediatric trauma score, systematically recorded PE findings, laboratory results, and injuries detected during hospitalization. Phase II: To confirm the sensitivity of the PE and U/A found in phase I, the model was applied to 91 additional trauma patients identified by International Classification of Diseases, 9th revision (ICD-9) codes as having IAI. INTERVENTION: None. RESULTS: Phase I: A total of 3939 tests were ordered for the 285 patients entered in phase I. Aspartate aminotransferase and alanine aminotransferase values were obtained in 59% of patients; glucose level was obtained in 78% of patients; complete blood cell count, U/A, and levels of electrolytes, blood urea nitrogen, creatinine, amylase, and lipase were obtained in more than 85% of patients. The overall prevalence of laboratory abnormalities was 5.7%. Fourteen patients (4.8%) were identified who had a total of 23 significant IAIs (9 pancreatic, 6 splenic, 5 renal, 3 hepatic). The PE combined with U/A showing more than five red blood cells per high-power field had a sensitivity of 100%, specificity of 64%, positive predictive value of 13%, and negative predictive value of 100% for the detection of IAI. The presence of laboratory abnormalities suggesting injury did not increase the sensitivity of the model and significantly decreased both specificity and positive predictive value. Phase II: The PE combined with U/A identified an abnormality in 89 (97.8%) of 91 cases (95% confidence interval = 94.8% to 100%). CONCLUSIONS: In the moderately injured pediatric trauma patient, (1) there is a low prevalence of laboratory abnormalities; (2) the PE combined with U/A is a highly sensitive screen for IAI; and (3) in patients with a normal PE of the abdomen and a normal U/A, laboratory testing seldom identifies unsuspected IAI.

Reovirus-induced liver disease in severe combined immunodeficient (SCID) mice. A model for the study of viral infection, pathogenesis, and clearance.

Adult severe combined immunodeficient (SCID) mice can be infected by the oral route with reovirus, and a systemic infection can be established. Infectious virus is recovered from all internal organs, and the mice die in 4-6 wk. Chronic, discrete inflammatory lesions appear in the liver of infected mice, and are associated with hepatocytes containing demonstrable levels of viral antigen. The adoptive transfer of Peyer's patch (PP) cells from congenic mice before infection protects the SCID mice against disease and death. Immune donor PP cells can be distinguished from nonimmune cells by their ability to contain and resolve infection by 1 wk after challenge.

Reoviruses as probes of the gut mucosal T cell population.

Reovirus, serotype 1, causes a transient, asymptomatic infection of the murine intestine when given intraduodenally or orally. However, this infection markedly perturbs both B- and T- cell populations in Peyer's patches (PP) resulting in: 1) a rapid and persistent increase in specific precursors for cytotoxic T cells (pCTL) and a gradient of frequencies highest in PP and lowest in distal lymphoid tissue; 2) a similar increase in memory B cells committed to IgA; 3) the transient appearance of a subset of germinal center B cells identified by MAb, GC-T; 4) the appearance of pCTL among intraepithelial lymphocytes; and 5) the antigen non-specific alteration in Ig isotype potential of B cells previously primed and found in PP. The pCTL appearing upon acute gut mucosal infection with reovirus are Thyl+, Lyt2+, virus-specific, viral serotype non-specific, class I MHC haplotype restricted and occur within the subset of T cells which newly appears also identified by MAb GC-T. Infections of both neonatal and severe-combined immunodeficient mice indicate that the elements of the immune system may operate at many levels to resist, limit, contain, and resolve viral infection.