Ascending nonobstructive pyelonephritis was produced in nonhuman primates by ureteral catheterization which delivered Escherichia coli (04:H1) to the renal pelvis while creating intrarenal reflux. Female rhesus monkeys (Macaca mulatta) were immunosuppressed by cyclophosphamide before infection and weekly thereafter and compared to those with infection only. Kidney tissue was examined by electron microscopy in an effort to compare the development of the infection in the two groups of monkeys, i.e., immunocompetent and immunosuppressed. Reorganization of bacterial cytoplasm into small dense bodies (averaging 250 A in diameter) was seen in two of the suppressed animals. These particles were within bacteria that were either free in the medullary interstitium or in macrophages. Clusters of electron-dense bodies of the same size and morphology were also seen within subendothelial spaces of glomerular capillaries. Protoplast-like forms were observed within the medullary interstitium. One cell wall-less form contained particles (as previously described) within a large peripheral vesical. Gross pyelonephritic scarring occurred in all immunosuppressed animals. This study has shown morphologically that classical bacterial organisms placed into the intact kidneys of partially immunoincompetent nonhuman primates will cause pyelonephritis and continue to exist for 18 days. These observations of the futile efforts by suppressed populations of leukocytes to clear intrarenal bacteria raise interesting questions about the host-paradise relationship in chronic renal infection.