Experimental urinary tract infection with Pseudomonas aeruginosa in mice

We have studied the host defense factors that operate during the course of chronic respiratory tract infection caused by Klebsiella pneumoniae 27 in CBA/J mice. A large number of polymorphonuclear leukocytes (PMNs) rapidly infiltrated the alveolar spaces after infection.Treatment with cyclophosphamide (CY) before infection greatly reduced the infiltration of PMNs and caused an increase in bacterial counts.CY treatment of mice in the chronic phase also caused bacterial proliferation in the lungs. The administration of a high titer immune serum efficiently reduced the bacterial counts in the lungs during the early phase but not during the chronic phase.The proliferation of bacteria induced by CY treatment was not suppressed by the administration of the immune serum in either phase. When the mice were exposed to an aerosol containing Pseudomonas aeruginosa P9 in the chronic phase, the organisms from the secondary infection were eliminated from the lungs in the same manner as in the case of primary infection with P. aeruginosa. Thus, PMNs seem to play an important role in the suppression of bacterial proliferation in the early and chronic phases, and the specific antibody might have a supplementary effect on the defensive action of PMNs in the chronic phase.It is also presumed that the bacteria in the chronic phase of infection are sequestered at sites hardly accessible to PMNs.Although many antimicrobial agents are now available, chronic infections are still difficult to cure. Chronic infection models are therefore required to examine the host-parasite relationship in the chronic phase.We have previously established a model of chronic respiratory tract infection in mice caused by Klebsiella pneumoniae (11). The course of infection in this model is highly reproducible, and the bacterial counts in the lungs after infection change with time, showing four different phases. In the first phase, the bacterial counts decrease for 4 days. In the second phase, the bacterial counts increase starting day 4 and reaching the initial level 1 week after infection. The third phase lasts from 1 week to 4 weeks after infection, during which time the bacterial counts remain relatively unchanged. The fourth phase starts 4 weeks after infection, and thereafter the bacterial counts gradually increase. This model is useful for analyzing 615

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“…Agglutination test. Serum agglutinating antibody against K. pneumoniae 27 was examined by the microtiter method as described previously (14).…”

Section: Methodsmentioning

confidence: 99%

Examination of Host Defense Factors Responsible for Experimental Chronic Respiratory Tract Infection Caused by Klebsiella pneumoniae in Mice

Iizawa

Nishi

Kondo

et al. 1991

Microbiology and Immunology

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“…Marked ulceration of the bladder after pseudomonas infection has been (Hematoxylin and eosin stain; xl,OOO, approximately) described in rats with prior injury of the bladder wall (14). Other studies of the histological changes in the bladder have not noted ulceration with pseudomonas (13) or Escherichia coli (3,15). In preliminary studies, we have observed ulceration of bladder in mice after injection of E. coli (unpublished observations).…”

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confidence: 97%

“…Experimental studies of the urinary tract have dealt mainly with the kidney infections associated with pseudomonas infection (4,6,7,13). There have been few clinical or experimental studies of pseudomonas infection in the lower urinary tract.…”

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confidence: 99%

Pseudomonas urinary tract infection in mice

Montgomerie¹,

Tuddenham²,

Howard³

et al. 1980

Infect Immun

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When Pseudomonas aeruginosa was injected through a catheter into the bladder, hemorrhage, edema, and vessel engorgement were seen 1 h after challenge. At 3 hours we observed microulceration of the bladder, which rapidly healed and was rarely present after 24 h. Pseudomonas was cultured from 50% of the kidneys at 1 week, and the number of kidneys infected decreased over 4 weeks.Pseudomonas aeruginosa urinary tract infections have been a frequent problem in nosocomial infections. Bacteremia may occur with lower urinary tract manipulation, and ascending urinary tract infection may result in pyelonephritis and renal damage.Experimental studies of the urinary tract have dealt mainly with the kidney infections associated with pseudomonas infection (4, 6, 7, 13). There have been few clinical or experimental studies of pseudomonas infection in the lower urinary tract. We have injected pseudomonas into the bladder through a urethral catheter, and we have observed the natural history of the bladder and renal infection using this technique. P. aeruginosa strain T2 (obtained from M. Fisher) was used. Swiss Webster female mice, weighing approximately 20 g, were anesthetized with ether, and 0.025 ml of pseudomonas, a washed overnight culture (adjusted to 2 x 108/ ml) was injected into the bladder through a urethral catheter (polyethylene tubing with an outside diameter of 0.061 cm, Clay Adams, New Jersey). Residual urine in the bladder was aspirated before the infection. Control mice were injected with phosphate-buffered saline.Mice were killed at intervals after the infection. At the time of sacrifice, the bacterial content of the kidney and the bladder was determined quantitatively. Any urine in the bladder was aspirated with a needle and syringe. The kidneys and bladder were removed aseptically and homogenized in broth. Serial dilutions were made in broth, and samples were plated in molten brain heart infusion (BHI) agar. Midcoronal sections of kidneys were placed in glutaralde-hyde fixative for histology. The bladder was also sectioned for histology. At the time of sacrifice, blood was obtained from the heart and inoculated into BHI broth. Table 1 shows the results of a study in which 5 x 106 pseudomonas cells were injected through a urethral catheter and the animals were killed at intervals up to 4 weeks after the injection. The maximum number of bacteria was seen in the bladder at 24 h and in the kidneys at 3 days. No mice died. The histological changes in the bladder are shown graphically in Fig. 1. The most marked changes in the bladder were seen at 4 h, the earliest time the bladder was examined in this experiment. Polymorphonuclear leukocyte (PMN) infiltration and edema of the submucosa was prominent, and focal ulceration of the mucosa and hemorrhage were seen in almost all the bladders (Fig. 2). In some ulcers, bacteria could be seen on the surface of the ulcer. Over 3 days, hemorrhage, ulceration, and edema rapidly decreased. The PMN infiltration of the bladder was maximal at 4 h and continued up to 1 week in some ...

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“…The low susceptibility to UTI in most laboratory animals has been an obstacle in the search for useful animal models. To cause the UTI in experimental animals by interrupting the host defense mechanisms, various researchers applied different treatments to increase the susceptibility by obstructions of the ureter (4) or urethra (17,24), kidney or bladder massage (3,11), implantation of a glass bead (25), injection of acid (6), the scars of antecedent bacterial infection (7,21), or glucose-induced diuresis (15).…”

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Establishment of a Mouse Model of Cystitis and Roles of Type 1 Fimbriated Escherichia coli in Its Pathogenesis

Liao

Tomochika

Watanabe

et al. 1992

Microbiology and Immunology

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The role of type 1 fimbriae in promoting bladder colonization and the course of Escherichia coli cystitis were examined with type 1 fimbriated strains of clinically isolated E. coli. In the experiments of mice in vivo, intact bladder epithelium showed natural resistance to the adherence of type 1 fimbriated and nonfimbriated E. coli. However, the exfoliation of bladder superficial cells by trypsinization before the bacterial inoculation promoted the adhesion and colonization of type 1 fimbriated E. coli onto bladder epithelium. After colonization of E. coli, maximum numbers of E. coli and leukocytes were observed 3 days after inoculation.Nine days after inoculation, both of E. coli and leukocytes disappeared and the regeneration of superficial cells was observed.On the other hand, superficial cells in mice injected with phosphate-buffered saline or non-fimbriated E. coli regenerated 5 days after trypsinization.The present study demonstrated that the removal of superficial cells is essential for the adhesion and colonization of type 1 fimbriated E. coli onto bladder epithelium in vivo and a new model of E. coli cystitis in mice was established.The model which we established is valuable for histopathological, immunological, and therapeutic studies.

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Experimental urinary tract infection with Pseudomonas aeruginosa in mice

Cited by 31 publications

References 13 publications

Examination of Host Defense Factors Responsible for Experimental Chronic Respiratory Tract Infection Caused by Klebsiella pneumoniae in Mice

Examination of Host Defense Factors Responsible for Experimental Chronic Respiratory Tract Infection Caused by Klebsiella pneumoniae in Mice

Pseudomonas urinary tract infection in mice

Establishment of a Mouse Model of Cystitis and Roles of Type 1 Fimbriated Escherichia coli in Its Pathogenesis

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