Subject(s)
Coinfection/diagnosis , Herpes Zoster/diagnosis , Influenza, Human/diagnosis , Streptococcal Infections/diagnosis , Superinfection/diagnosis , Tonsillitis/diagnosis , Adult , Ampicillin/therapeutic use , Anti-Bacterial Agents/therapeutic use , Antiviral Agents/therapeutic use , Coinfection/complications , Coinfection/microbiology , Coinfection/virology , Herpes Zoster/complications , Herpes Zoster/drug therapy , Herpes Zoster/virology , Humans , Influenza A virus , Influenza, Human/complications , Influenza, Human/drug therapy , Influenza, Human/virology , Male , Oseltamivir/therapeutic use , Streptococcal Infections/complications , Streptococcal Infections/drug therapy , Streptococcal Infections/microbiology , Superinfection/complications , Superinfection/microbiology , Superinfection/virology , Tonsillitis/complications , Tonsillitis/drug therapy , Tonsillitis/microbiology , Torso , Valacyclovir/therapeutic useABSTRACT
This study aimed to generate a mouse model of acquired glomerular sclerosis. A model system that allows induction of podocyte injury in a manner in which onset and severity can be controlled was designed. A transgenic mouse strain (NEP25) that expresses human CD25 selectively in podocytes was first generated. Injection of anti-Tac (Fv)-PE38 (LMB2), an immunotoxin with specific binding to human CD25, induced progressive nonselective proteinuria, ascites, and edema in NEP25 mice. Podocytes showed foot process effacement, vacuolar degeneration, detachment and downregulation of synaptopodin, WT-1, nephrin, and podocalyxin. Mesangial cells showed matrix expansion, increased collagen, mesangiolysis, and, later, sclerosis. Parietal epithelial cells showed vacuolar degeneration and proliferation, whereas endothelial cells were swollen. The severity of the glomerular injury was LMB2 dose dependent. With 1.25 ng/g body wt or more, NEP25 mice developed progressive glomerular damage and died within 2 wk. With 0.625 ng/g body wt of LMB2, NEP25 mice survived >4 wk and developed focal segmental glomerular sclerosis. Thus, the study has established a mouse model of acquired progressive glomerular sclerosis in which onset and severity can be preprogrammed by experimental maneuvers.
Subject(s)
Disease Models, Animal , Genetic Engineering , Glomerulosclerosis, Focal Segmental/physiopathology , Mice , Animals , Antibodies, Monoclonal , Exotoxins , Glomerulosclerosis, Focal Segmental/genetics , Glomerulosclerosis, Focal Segmental/pathology , Humans , Imaging, Three-Dimensional , Immunotoxins , Kidney/metabolism , Kidney/pathology , Kidney Glomerulus/ultrastructure , Mice, Transgenic , Microscopy, Electron , Microscopy, Electron, Scanning , Nephrotic Syndrome/chemically induced , Receptors, Interleukin-2/metabolism , Severity of Illness IndexABSTRACT
The authors describe a patient with osteosarcoma in whom a brain abscess developed after autologous peripheral stem cell transplantation. Serologic markers of fungal infection were negative, but fungal DNA was detected in the cerebrospinal fluid (CSF) by panfungal polymerase chain reaction (PCR) assay using primers derived from fungal 18S ribosomal RNA (rRNA) genes. The sequence of PCR products on the panfungal assay was identical to the 18S rRNA genes of Aspergillus species. The combination of sequence analysis and panfungal PCR assay could be useful in the diagnosis of cerebral aspergillosis.
