Endotoxin and nanobacteria in polycystic kidney disease.

BACKGROUND: Microbes have been suspected as provocateurs of polycystic kidney disease (PKD), but attempts to isolate viable organisms have failed. Bacterial endotoxin is the most often reported microbial product found in PKD fluids. We assessed potential microbial origins of endotoxin in cyst fluids from 13 PKD patients and urines of PKD and control individuals. METHODS: Fluids were probed for endotoxin and nanobacteria, a new bacterium, by the differential Limulus Amebocyte Lysate assay (dLAL), genus-specific antilipopolysaccharide (LPS) antibodies, monoclonal antibodies to nanobacteria, and hyperimmune serum to Bartonella henselae (HS-Bh). Selected specimens were also assessed by transmission electron microscopy (TEM) and nanobacterial culture methods. RESULTS: LPS or its antigenic metabolites were found in more than 75% of cyst fluids tested. Nanobacteria were cultured from 11 of 13 PKD kidneys, visualized in 8 of 8 kidneys by TEM, and immunodetected in all 13 PKD kidneys. By immunodetection, nanobacterial antigens were found in urine from 7 of 7 PKD males, 1 of 7 PKD females, 3 of 10 normal males, and 1 of 10 normal females. "Nanobacterium sanguineum" was dLAL positive and cross-reactive with antichlamydial LPS and HS-Bh. Some cyst fluids were also positive for LPS antigens from Escherichia coli, Bacteroides fragilis and/or Chlamydia, and HS-Bh, as were liver cyst fluids from one patient. Tetracycline and citrate inhibited nanobacterial growth in vitro. CONCLUSION: Nanobacteria or its antigens were present in PKD kidney, liver, and urine. The identification of candidate microbial pathogens is the first step in ascertaining their contribution, if any, to human disease.

Platelet ultrastructure of high-risk premature infants.

Hemorrhagic and thrombotic complications are common in the term and preterm infant. Limited information is currently available about neonatal platelet structure and function, and how these may predispose infants to bleeding problems. This study comparing platelet ultrastructure of 71 different term and preterm infants with that of 15 adult control subjects revealed certain platelet morphological differences. Specifically, the adult platelets had more pseudopods, larger glycogen deposits, more visible microtubular structure, markedly fewer alpha granules, and smaller areas/perimeters than the infant platelets. Also, in infants greater than 31 weeks gestation, the platelets of vaginally-delivered infants were larger than those of both infants delivered by C-section and normal adults. These differences in platelet size and morphology may be related to developmental differences and/or the stress of delivery. These findings provide a framework for further exploration of neonatal platelet structure and function.