Performance of the ImmuView and BinaxNOW assays for the detection of urine and cerebrospinal fluid Streptococcus pneumoniae and Legionella pneumophila serogroup 1 antigen in patients with Legionnaires' disease or pneumococcal pneumonia and meningitis.

The performances of the ImmuView Streptococcus pneumoniae (Sp) and Legionella pneumophila (Lp) urinary antigen test were compared to that of the BinaxNOW Sp and Lp assays, using frozen urine from 166 patients with Legionnaires' disease (LD) and 59 patients with pneumococcal pneumonia. Thirty Sp-positive or contrived cerebrospinal fluids (CSF) were also tested. Test specimens were collected and tested at different sites, with each site testing unique specimens by technologists blinded to expected results. No significant differences in test concordances were detected for the ImmuView and BinaxNOW assays for the Sp or Lp targets for urine from patients with pneumococcal pneumonia or LD when performance from both sites were combined. At one of two test sites the ImmuView Lp assay was more sensitive than the BinaxNOW assay, with no correlation between test performance and Lp serogroup 1 monoclonal type. Urines from six of seven patients with LD caused by Legionella spp. bacteria other than Lp serogroup 1 were negative in both assays. Both tests had equivalent performance for Sp-positive CSF. The clinical sensitivities for pneumococcal pneumonia were 88.1 and 94.4% for the ImmuView and Binax assays, and 87.6 and 84.2% for the Lp assays, respectively. Test specificities for pneumococcal pneumonia were 96.2 and 97.0% for the ImmuView and Binax assays, and 99.6 and 99.1% for the Lp assays. Both assays were highly specific for Sp in pediatric urines from children with nasopharyngeal colonization by the bacterium. ImmuView and BinaxNOW assay performance was equivalent in these studies.

Microalbuminuria: an index of severity in childhood meningitis.

Urinary albumin excretion (AE) was determined by a sensitive method (below dipstick positive values, 15 to 300 micrograms/minute) in 68 children with meningitis during 48 hours after hospital admission; 51 children had bacterial meningitis (BM) and 17 had aseptic meningitis. AE (results as mean +/- SD) during 0 to 24 hours was higher (P < 0.001) in patients with BM (36 +/- 40 micrograms/minute) than with aseptic meningitis (7 +/- 5 micrograms/minute), albeit no cutoff value distinguished the two conditions accurately. In BM the clinical course (uneventful, intermediate, complicated, fatal) correlated with AE of 0 to 24 hours (r = 0.34, P < 0.05) and AE of 25 to 48 hours (r = 0.63, P < 0.001). Cerebrospinal fluid protein concentration 24 to 36 hours after initiation of treatment correlated with AE of 25 to 48 hours (r = 0.34, P < 0.05). An index obtained by dividing AE by the weight of the child predicted the severity of clinical course more precisely (77% sensitivity, 85% specificity) than AE alone. Hence renal AE is an easily and non-invasively determined acute phase reactant of potential value as an early estimate of severity of BM.

Long term monitoring of immunoreactive endothelin-1 and endothelin-3 in ventricular cerebrospinal fluid, plasma, and 24-h urine of patients with subarachnoid hemorrhage.

Endothelins (ETs), peptides that were originally isolated from endothelial cells, have extremely potent and long-lasting vasoconstricting effects on cerebral vessels in vitro and in vivo. Observations that astrocytes produce these peptides and that their ET production can be stimulated, e.g. by thrombin, and potentiated via a self-enhancing autoregulatory mechanism may have shed new light upon the pathogenesis of cerebrovasospasm (CVS). ETs are present at low levels in normal human cerebrospinal fluid (CSF). Few and contradictory reports exist on ET levels in subarachnoid hemorrhage (SAH)-associated CVS. We monitored ventricular CSF, plasma, and 24-h urine levels of immunoreactive endothelin-1 (ET-1) and endothelin-3 (ET-3) in seven patients with SAH, who did (five) or did not (two) develop CVS in the course of their disease, as well as in two patients with different conditions (acoustic neuroma/postoperative meningitis; hydro-/hematocephalus) over 7-19 days. A distinct peak of both ET-1 and ET-3 in CSF of patients with SAH coincided with clinically documented signs of CVS and was absent in CSF of patients with SAH but no CVS. CSF levels of ET-1 and ET-3 displayed a striking parallelism in all subjects. Plasma ET-1 levels were essentially in the normal range. ET-3 was not detectable in plasma under our assay conditions. The excretion profiles of ET-1 and ET-3 in 24-h urine revealed again a predominantly parallel behavior of the two peptides. Interestingly, patients with high ET levels in CSF showed simultaneous peaks in urinary ET excretion, expressed as nanograms per gram of creatinine. Our findings support an association of ETs with the pathogenic events following SAH. The well-documented effects of these peptides on cerebral vessels suggest they are mediators rather than markers of disease.

Vasopressin levels in infants during the course of aseptic and bacterial meningitis.

We measured urine vasopressin (VP) once daily on days 1 through 3 in 18 patients hospitalized with meningitis. Urine VP values were 215 +/- 100, 116 +/- 44, and 69 +/- 23 pg/mL on days 1 through 3, respectively, for children with bacterial meningitis and 34 +/- 14, 20 +/- 4, and 15 +/- 4 pg/mL for those with aseptic meningitis. Urinary VP levels of infants with bacterial meningitis were significantly greater than those of healthy ambulatory subjects (n = 18) on all three study days; VP values of infants with bacterial meningitis were also greater than those of infants with aseptic meningitis on study days 2 and 3. The VP levels for the subjects with aseptic meningitis were significantly greater than those of the controls on day 1 only. None of the infants exhibited the clinical syndrome of inappropriate antidiuretic hormone secretion.

Unsuspected bacterial infections in febrile convulsions.

In a 12-month prospective study in 1984, blood and urinary cultures were obtained as a routine from 307 children who presented with fever and convulsions to the Mater Misericordiae Children's Hospital, Brisbane, and the results were compared with data from 1981-1983 when cultures were not taken as a routine. In the prospective study, bacteraemia was found in 12 (4.3%) of 282 patients but was not suspected clinically in half of these; urinary-tract infection was found in seven (2.6%) of 272 patients and in six of these it was not suspected clinically. All 12 patients with unsuspected bacteraemia or urinary-tract infection had persistent fever; of these, nine patients suffered simple convulsions and all cases of urinary-tract infection occurred in female patients. Bacteraemia was significantly more common in patients of less than two years of age, in children who were selected for lumbar puncture and in the study period compared with the retrospective period, 1981-1983. Leukocytosis (white-cell count, more than 15.0 X 10(9)/L) was a sensitive (75%) diagnostic aid but was poorly specific (59%) for bacteraemia. Bacterial meningitis was not diagnosed initially in four of the nine cases which occurred among children who presented with fever and convulsions between 1981 and 1984; in all four children, the cerebrospinal fluid appeared normal at hospital admission. We conclude that bacteraemia and urinary-tract infections are detected more frequently in children who are admitted to hospital with febrile convulsions when cultures are performed as a routine. In the at-risk group (children of less than two years of age), the prevalence of urinary-tract infection is increased in female patients and the prevalence of bacteraemia is increased in those patients who are selected for lumbar puncture. The use of leukocytosis as a criterion to determine the need for blood cultures improves the diagnostic yield but would result in increased costs and additional venepuncture. Bacterial meningitis was rare in our case series and the performance of a lumbar puncture as a routine at admission to hospital would not have led to its earlier diagnosis.

Inappropriate antidiuretic hormone in children with viral meningitis.

Urinary excretion rates of antidiuretic hormone were determined by radioimmunoassay in children with bacterial (6) and viral (11) meningitis, and in children with other febrile illnesses (7). These values were compared to normal data obtained from 50 healthy, normally hydrated children ranging in age from 1 week to 9 years. Plasma sodium concentrations were measured in the sick children; urine osmolality and creatinine concentrations were measured in all children. Upon admission, all children with bacterial meningitis and 64% of those with viral meningitis had urinary antidiuretic hormone excretion rates greater than 2 S.D. above values obtained from age-matched controls. Fifty-seven percent of children with other febrile illnesses had similarly elevated antidiuretic hormone values; however, only in the bacterial and viral meningitis groups were antidiuretic hormone excretion rates inappropriate because they occurred when serum sodium concentrations were found to be normal or low normal (i.e., 136 +/- 2 mEq/L and 137 +/- 1 mEq/L, respectively). The average serum sodium in the group with other febrile illnesses was higher (146 +/- 5 mEq/L; p less than 0.05) and could represent an appropriate stimulus for antidiuretic hormone release. In spite of high levels of antidiuretic hormone, most viral meningitis patients did not concentrate their urine, probably because all except 2 were younger than 2 months of age. We conclude that viral meningitis, like bacterial meningitis, frequently is associated with inappropriate antidiuretic hormone secretion; however, most children with viral meningitis may be protected from developing hyponatremia because of their inability to concentrate their urine.

Cellular elements in the urine in health and in acute infectious diseases, especially with respect to the presence of haematuria. A study with application of millipore procedure and Papanicolaou staining.

The excretion of cellular per litre of urine amounted in healthy persons to, in round figures, one million epithelial cells (2.5 cells per visual field) in both sexes, one million leukocytes in males, one million erythrocytes in females and 0.5 million in males. The maximal excretion was calculated to be 5-6 million per litre. In acute infections the number of epithelial cells and leukocytes in the urine rose to more than the double. Pathological microscopic haematuria, judged by exceeding of the maximal value for normal excretion during the acute phase (24 or more erythrocytes per visual field), occurred in no case of mycoplasma infection, in about 4% of measles, mononucleosis, serous meningitis and hepatitis cases, in about 8% of mumps and streptococcal infections, and in more than 20% of influenza A2 cases. Statistical significance or probable significant existed between influenza and other diseases. The haematuria was unrelated either to the general degenerative or to the specific inclusion-provocative reaction within the renal and urinary tract epithelium. The cause is sought in an involvement of glomeruli with increased diapedesis. The special position of influenza may be explained by the marked haemorrhagic reactions produced by this infection. In one case persistent haematuria combined with increased content of inclusion-bearing cells occurred after influenza. Immunoglobulin deposition in glomerular mesangium may perhaps be one explanation of this haematuria.