Sterile cerebrospinal fluid pleocytosis in young infants with urinary tract infection.

BACKGROUND: During the first 3 months of life febrile infants are subjected to sepsis workup, which includes evaluation for urinary tract infection (UTI) and meningitis. We investigated the existence of concomitant meningeal inflammation in infants younger than 90 days old affected with UTI. METHODS: We reviewed the medical records of all infants younger than 90 days old, who were hospitalized for UTI from January, 1990, to January, 2001. For the diagnosis of sterile cerebrospinal fluid (CSF) pleocytosis, the child's age, the CSF total white blood cell (WBC) count and the CSF absolute neutrophil count were taken into consideration. CSF pleocytosis was defined as the presence of > or = 35, > or = 21 and > or = 15 WBC/mm3 of CSF during the first, second and third month of life, respectively. The CSF Gram-stained smear, latex agglutination test and bacterial culture were negative. RESULTS: Sterile CSF pleocytosis was found in 15 (12.8%) of 117 infants with UTI who had had a lumbar puncture included in their initial laboratory evaluation. The 15 infants had a median age +/- semiinterquartile range of 40 +/- 25 days (range, 4 to 75 days). In these infants the median CSF WBC count +/- semiinterquartile range was 55 +/- 125/mm3 (range, 21 to 1,270/mm3). CONCLUSIONS: Sterile CSF pleocytosis was found in 12.8% of infants younger than 90 days old with UTI. The pathogenesis of this meningeal inflammation is not fully understood. Although bacterial infection of the subarachnoid space, with low bacterial seeding, cannot be excluded, at least in some cases, it is possible that CSF pleocytosis in some of the infants with UTI is mainly caused by the endotoxin of Gram-negative or other inflammation-inducing molecules of Gram-positive urine pathogens.

Detection of hepatitis B virus DNA in blood units with anti-HBc as the only positive serological marker.

Serum samples from 10,629 blood donors were screened for hepatitis B virus (HBV) serological markers (HBsAg, anti-HBs, anti-HBc, anti-HBc IgM), anti-HCV, anti-HIV1/2 and ALT. Seventy five (0.7%) blood donors were found HBsAg-positive, 1,543 (14.5%) were carrying both anti-HBc and anti-HBs. whereas 507 (4.8%) samples were positive only for anti-HBc. Among the group of 507 anti-HBc positive samples, 303 were obtained from regular volunteer blood donors who were studied in two separate time intervals of at least 6 months' duration, and 204 were from first-time blood donors. The possibility of post-transfusion hepatitis B after donation of these 507 blood units was studied by determining the presence of HBV DNA as a marker of viral replication and infectivity. HBV DNA was detected by two methods (i) a chemiluminescent molecular hybridization assay, (ii) polymerase chain reaction (PCR) followed by DNA enzyme immunoassay (DEIA). Six out of 507 samples exhibited HBV DNA results in the gray zone of the hybridization assay, but were confirmed as negative by PCR DEIA. The other 501 samples were HBV DNA-negative by both methods, although 36 of them had increased ALT levels. No cases of post-transfusion hepatitis B were reported during the year in which these 501 blood units were provided. These results show that blood units which were positive only for anti-HBc, with normal ALT and were HBV DNA-negative may be considered not infectious for hepatitis B. Gray zone results of HBV DNA using hybridization quantitative assay must be confirmed as positive or negative by a more sensitive method such as PCR. Blood units which are anti-HBc-positive, with increased ALT levels and are HBV DNA-negative, which appear to not be related to HBV replication and infectivity, may be not safe for donation because of the potential existence of other as yet unknown, hepatotropic viruses.