Skip to main content
The Journal of Experimental Medicine logoLink to The Journal of Experimental Medicine
. 1956 Nov 30;104(6):803–815. doi: 10.1084/jem.104.6.803

EXPERIMENTAL PYELONEPHRITIS

I. EFFECT OF URETERAL LIGATION ON THE COURSE OF BACTERIAL INFECTION IN THE KIDNEY OF THE RAT

Lucien B Guze 1, Paul B Beeson 1; With the Technical Assistance of Elizabeth R. Maloney1
PMCID: PMC2136652  PMID: 13376805

Abstract

A study has been made of the effect of ureteral ligation on the susceptibility of the kidney to pyogenic infection. In most experiments a strain of E. coli was employed as the test organism, being injected intravenously in varying quantity either before or after ureteral ligation. A few experiments were also carried out with S. marcescens. Preliminary observations were made on the distribution and persistence of E. coli following its inoculation into the blood stream of normal rats. Rapid reduction in number of bacteria in the circulation occurred during the first 30 minutes, but bacteriemia persisted at a comparatively low level for at least 48 hours. Large proportions of the inoculated bacteria were arrested and apparently destroyed in the liver, spleen, and lungs. Comparatively small numbers were deposited in the kidneys; nevertheless, these continued to be demonstrable during the 1st week, without notable tendency to increase or decrease, then disappeared during the 2nd week. There was no acceleration in rate of disposal of the bacteria in the kidney when a second injection was made 1 week after the first. In rats with one ureter ligated the number of bacteria lodging in the kidneys after intravenous inoculation did not differ from that found in normal animals. It appears, therefore, that the increased susceptibility of the obstructed kidney to infection via the blood stream is not attributable to an increased trapping of circulating bacteria. 4 to 6 hours after the intravenous injection, however, an increased number of bacteria could be demonstrated in the obstructed kidney, apparently due to local multiplication, and by the end of 24 hours purulent infection was usually obvious. A comparatively large number of bacteria was required to cause infection, even in the kidney with obstruction. This appeared to be related to the small proportion of the intravenous inoculum which lodged in the kidney initially. Although bacteria could be demonstrated in the normal kidney for a week or more following intravenous injection it was not possible to induce active infection with equal regularity by ligating the ureter throughout this time. During the first 3 days the majority of obstructed kidneys developed infection, but after 5 or more days this occurred in only a small proportion of animals so treated. The reason for the difference, in relation to interval between intravenous injection and time of ligation, is not apparent. When the ureter was ligated but no intravenous injection of bacteria was given, staphylococcal infection developed in the obstructed kidney within 2 weeks in about one-third of the animals. Reasons are given for the belief that this was blood-borne infection, and not the result of contamination at the time of operation. Staphylococci were not recovered from the normal rat kidney. These "spontaneous" staphylococcal infections seldom developed when E. coli was injected intravenously at the time of ureteral ligation.

Full Text

The Full Text of this article is available as a PDF (773.3 KB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. BEESON P. B. Factors in the pathogenesis of pyelonephritis. Yale J Biol Med. 1955 Nov;28(2):81–104. [PMC free article] [PubMed] [Google Scholar]
  2. Bradley S. E., Chasis H., Goldring W., Smith H. W. HEMODYNAMIC ALTERATIONS IN NORMOTENSIVE AND HYPERTENSIVE SUBJECTS DURING THE PYROGENIC REACTION. J Clin Invest. 1945 Sep;24(5):749–758. doi: 10.1172/JCI101660. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. DUBOS R. J., SCHAEDLER R. W. Reversible changes in the susceptibility of mice to bacterial infections. I. Changes brought about by injection of pertussis vaccine or of bacterial endotoxins. J Exp Med. 1956 Jul 1;104(1):53–65. doi: 10.1084/jem.104.1.53. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. PILLEMER L., SCHOENBERG M. D., BLUM L., WURZ L. Properdin system and immunity. II. Interaction of the properdin system with polysaccharides. Science. 1955 Sep 23;122(3169):545–549. doi: 10.1126/science.122.3169.545. [DOI] [PubMed] [Google Scholar]
  5. ROWLEY D. Stimulation of natural immunity to Escherichia coli infection: observations on mice. Lancet. 1955 Jan 29;268(6857):232–234. doi: 10.1016/s0140-6736(55)90163-x. [DOI] [PubMed] [Google Scholar]
  6. SPITZNAGEL J. K., SCHROEDER H. A. Experimental pyelonephritis and hypertension in rats. Proc Soc Exp Biol Med. 1951 Aug;77(4):762–764. doi: 10.3181/00379727-77-18919. [DOI] [PubMed] [Google Scholar]
  7. THOMAS L. The physiological disturbances produced by endotoxins. Annu Rev Physiol. 1954;16:467–490. doi: 10.1146/annurev.ph.16.030154.002343. [DOI] [PubMed] [Google Scholar]

Articles from The Journal of Experimental Medicine are provided here courtesy of The Rockefeller University Press

RESOURCES