Experimental Hematogenous Pyelonephritis Research Articles

Local immune response to Escherichia coli pili in experimental pyelonephritis.

The local immune response to pili of Escherichia coli O6:K13:H1 was determined in experimental hematogenous pyelonephritis in rabbits. Pili purified from sheared cells by ammonium sulfate precipitation were found to be pure by electron microscopy and negative for lipopolysaccharide by limulus lysate assay. Antipilus antibody was detected in serum and newly synthesized protein from infected animals with enzyme-linked immunosorbent assay. Serum and local (intrarenal) antibodies were of the immunoglobulin G class, were detectable by day 20 of infection, and persisted though 250 days of infection. These data suggest that pili are present on the organism at the site of infection, since they induce the local synthesis of antipilus antibody in experimental pyelonephritis.

Virulence of Escherichia coli in experimental hematogenous pyelonephritis in mice

Differences in nephropathogenicity between Escherichia coli strains were studied by following the kinetics of the viable count in the mouse kidney during 8 h after intravenous injection. Assuming as a reference point that at zero time 0.1% of the inoculum was lodged in the kidney, we found that strains fell into three main groups with different behavior patterns: in group I, the viable count fell and remained low; in group II, the viable count first fell and then rose after 4 h, reaching the level of the reference point within 8 h; in group III, the viable count rose rapidly and remained high. The kinetics of the viable counts were also studied in blood, spleen, and liver: group I and II strains behaved similarly; only in the kidney did group II strains show higher counts than group I strains. These data suggest that group II strains are specifically virulent for the mouse kidney. Group III strains also gave higher viable counts in blood and spleen but comparable counts in the liver, suggesting that group III strains are more generally virulent. Fifty percent lethal dose measurements confirmed the conclusion that group I strains are avirulent and group III strains are the most virulent. Possible relationships between behavior pattern and serotype are discussed.

Local immune response to lipoprotein of the outer membrane of Escherichia coli in experimental pyelonephritis

The local immune response to the lipoprotein of the outer membrane of Escherichia coli O6:K13:H1 was determined in experimental hematogenous pyelonephritis in rabbits. Local antibody was analyzed with the enzyme-linked immunosorbent assay on newly synthesized protein from kidney. Local or intrarenal antibody was detected by day 7 of infection, a few days later than serum antibody. The synthesis of antibody in immunoglobulin G class was present 6 days before the synthesis of immunoglobulin M antibody. Antibody activity to this antigen was also present in urine, and antibody could be eluted from bacteria coated with antibody. Local antibody to the lipoprotein was synthesized in equal quantities by animals infected with a heterologous species of E. coli. This antigen was not as mitogenic for splenic or kidney lymphocytes as was the O antigen. Hence, the lipoprotein of the organisms is a potent immunogen but a weak mitogen locally in pyelonephritis. This antibody response probably does not induce protection against infection, but represents a marker for presence of infection.

The local immune response to Escherichia coli O and K antigen in experimental pyelonephritis.

Although the systemic and local immune response to the O antigen of Escherichia coli has been well characterized, little information is available on the immune response to K anigen. Experimental hematogenous pyelonephritis was produced with Escherichia coli 06 K13 H1 and the serum and local (intrarenal) antibody response to O and K antigens was determined with the enzyme-linked immunosorbent assay. Both local and serum antibody responses to the K antigen were significantly less than that to the O antigen. The K antigen induced low titer IgM and IgG antibody responses in fewer than one-half of the animals and did not induce a local IgA response in any animal. In contrast, the O antigen induced local antibody responses in each of the immunoglobulin classes in all animals from day 9 of infection. Similarly, the serum IgM and IgG antibody titers to the K antigen were significantly less than those evoked in response to the O component of the Escherichia coli. No serum IgA anti-K antibodies were detected. These observations helf clarify the roles of these two antigens in pyelonephritis. Although the K antigen of Escherichia coli functions as a virulence factor in upper urinary tract infections, this antigen does not elicit a significant immune response, whereas the O antigen does induce a significant antibody response which could be of protective or diagnostic benefit.

Preventive effects of trimethoprim/sulphamethoxazole on experimental staphylococcic pyelonephritis in rats.

108 white rats weighing 170-250 G were given trimethoprim, sulphamethoxazole and the combination trimethoprim 1/sulphamethoxazole orally and parenterally in order to test the preventive effect of these substances on experimental hematogenous pyelonephritis due to Staphylococcus aureus. Oral applications of 48 mg/kg/24h of trimethoprim/sulphamethoxazole prevented abscess formation. Intraperitoneal applications of 48mg/24h of the combination did not seem as effective as the oral applications. On the other hand, there was no difference between the effects of oral and parenteral applications when the doses were 96 mg/kg/24h. The preventive effects of trimethoprim and sulphamethoxazole alone were much less than those observed when the combination trimethoprim/sulphamethoxazole was given. No peritoneal or other tissue damage was observed after intraperitoneal injections of trimethoprim/sulphamethoxazole in rats.

Experimental hematogenous pyelonephritis due to Escherichia coli in rabbits: the antibody response and its protective capacity.

Experimental hematogenous pyelonephritis due to Escherichia coli in rabbits: the antibody response and its protective capacity.

Effects of a new sulfonamide combination on experimental pyelonephritis.

Preventive effect of a sulfamethizole-sulfaethidole combination on experimental hematogenous pyelonephritis was examined on 120 white rats weighing 200–250 g. Two strains of <i>Staphylococcus aureus</i>, one of which was resistant to the combination and the other sensitive, and a resistant enterococcus strain were used for experimental hematogenous pyelonephritis. As a result, we observed that this kind of sulfonamide combination improved the pathomorphological lesions only in the group in which experimental pyelonephritis was produced by sensitive <i>S</i>. <i>aureus</i>. In the other groups, practically no positive effect could be seen.

Experimental Escherichia coli pyelonephritis: formation of spheroplasts in the kidney of the untreated rat.

An experimental hematogenous pyelonephritis produced in the rat byEscherichia coli was studied from the point of view of the possible role of L-forms of bacteria in chronic renal infection. Osmotically fragile cells were shown in the kidneys from the 3rd day after inoculation, and their percentage of the totalE. coli cell number increased during the course of the infection. In order to distinguish bacteria and spheroplasts of theE. coli strain used, two more methods were elaborated: 1) a bacteriological method based on the different sensitivity of bacteria and spheroplasts to erythromycin; this method confirmed the results obtained with osmotic shock; 2) an immunological method, using the indirect fluorescent antibody technique and an antiserum specifically labelling the spheroplasts; in kidneys removed 10–15 days after the inoculation, spherical bodies with morphological and antigenic characteristics similar to those of spheroplasts became visible.

Pyelonephritis. X. Microbial interference in streptococcal infections in the rat kidney.

Abstract Interactions of bacteriocin-producing strains of Streptococcus faccalis were studied in vitro and in vivo. In addition, experiments were done to evaluate the effect of physico-chemical parameters unique to the kidney on interactions of selected organisms. This was accomplished by incorporation of sodium or potassium chloride, urea, creatihine, varying pH, and increasing osmolality of the agar (sucrose). Effect of excess glucose as an energy source was evaluated. While results did not follow a predictable pattern, both increase and decrease in inhibition could be demonstrated, depending on combination of organisms used and parameter studied. Studies in vivo were done with experimental hematogenous pyelonephritis in the rat. The bacteriocin-producing strain ( S. faecalis variety (var.) zymogenes ) was able to inhibit but never completely eliminate susceptible S. faecalis G-K whether given one week prior to, simultaneously with, or one week after the G-K strain. When given simultaneously, it also predominated over another susceptible strain, ATCC 9790. However, with the less susceptible strain 3256, the results in vivo did not parallel those noted in vitro as the susceptible strain became more numerous. When S. faecalis var. zymogenes was given simultaneously with strain 2866 which was resistant to it in vitro, the latter at first predominated, but subsequently kidney bacterial populations tended to equalize. These data suggest that bacteriocin production and susceptibility thereto play an important role in determining the result of mixed renal infection. However, effect of physico-chemical characteristics of the kidney environment on bacteriocin activity may determine final outcome.

Localization and fate of Escherichia coli in hematogenous pyelonephritis.

1. Hematogenous E. coli pyelonephritis was produced in rats. The localization of the organisms and the persistence of bacterial antigens was followed by fluorescent antibody techniques as well as by standard histological and bacteriological methods. 2. Salient sequential features were as follows: Single organisms passed through vessel walls into the renal interstitium and began multiplication and subsequently evoked a leucocytic response. Bacterial multiplication did not occur in glomeruli or renal tubular cells. Bacteria did not appear within renal tubular lumina until microabscesses were well developed in the renal interstitium. Bacteriuria appeared late and represented secondary invasion rather than filtration of organisms. The infection healed spontaneously but, while sterile, the parenchymal scars contained large amounts of residual bacterial antigen. The persistence of bacterial antigen did not result in continuing inflammatory changes or progressive scarring. 3. The persistence of bacterial antigens is postulated to constitute a major antigenic stimulus responsible for active immunity in experimental hematogenous pyelonephritis.

The role of immunity in the pathogenesis of experimental hematogenous pyelonephritis.

Hematogenous pyelonephritis was produced in rats utilizing multiple strains of Escherichia coli, a strain of Klebsiella pneumoniae, and a strain of Proteus mirabilis. Three patterns of hematogenous pyelonephritis occurred which represent an interrelationship between an immune response to the infecting bacteria and the development of obstructive uropathy as a consequence of infection. First, the course of pyelonephritis due to strains of Escherichia coli was acute, self-limited, and associated with the development of circulating agglutinins. Following healing, this pattern of infection was associated with acquired resistance to reinfection with the same bacterial strain. Second, the course of pyelonephritis due to a strain of Klebsiella pneumoniae type C was chronic. This infection was not associated with the production of circulating agglutinins against encapsulated strains. Acquired resistance to reinfection by the homotypic strain could not be demonstrated following eradication of infection but was produced by the passive transfer of concentrated antiserum. Third, pyelonephritis due to Proteus mirabilis was associated with circulating agglutinins and resistance to reinfection with the same organism following eradication of infection, yet the course was chronic. The chronicity appeared to be the consequence of obstructive uropathy resulting from calculi which developed during the course of the infection. Resistance to reinfection was demonstrated in infections with strains of E. coli and P. mirabilis. The resistance is associated with specific immunity as demonstrated by the observation that: (a) it is type-specific, (b) it is of at least 3 months' duration, and (c) it can be passively transferred by means of rabbit antiserum. Since K. pneumoniae failed to evoke capsular antibodies in the rat, resistance to infection with K. pneumoniae was produced only by means of passively transferred concentrated rabbit antiserum and not by prior infection. Immunity can be demonstrated to have a significant role in the pathogenesis of experimental hematogenous pyelonephritis only in the absence of obstructive uropathy.

Reversible effects of myocardial ischemia in dogs

and its breakdown products in the course of experimental hematogenous pyelonephritis in rats was followed using, fluorescent antibody staining, routine histologic and bacteriologic technics. Early, bacteria are uniformly distributed within blood vessels of the kidneys. Within one hour, multiplication is observed and the bacteria invade vessel walls into the interstitial tissue. Organisms multiplying in the interstitial tissue produce microabscesses within eight hours. Bacteria within glomeruli may begin multiplication; however, within eight hours these organisms undergo degeneration and abscesses do not develop. With development of gross abscesses and scarring, morphologically discrete, viable Esch. coli disappear and progressive increase in amorphous endotoxin occurs. These observations demonstrate that bacterial endotoxin is present in progressively contracting kidneys and may play a role in evoking inflammatory changes as well as predisposing to subsequent localization of bacteria.