Biomedical subjects

D C Norman

Publications and source records attributed to D C Norman.

At least 19 recordsLinked to original sources

PubMed1992

Mechanism of immunosuppressive effect of alprazolam: alprazolam suppresses T-cell proliferation by selectively inhibiting the production of IL2 but not acquisition of IL2 receptor.

The purpose of this study was to elucidate the mechanism of action of alprazolam on concanavalin A (Con A)-induced murine T-cell proliferation. Splenic cells of BALB/c mice were first cultured with an optimum dose of Con A in the presence or absence of varying doses of alprazolam to assess effects of alprazolam on T-cell proliferation, interleukin 2 (IL2) production and IL2 receptor (IL2R) expression. Then, Con A-induced T-blast cells from BALB/c mice were cultured with an excess dose of human recombinant IL2 (rIL2) or crude rat IL2 supernate in the presence or absence of alprazolam to assess the effects of alprazolam on the interaction of IL2 and IL2R. The results of these studies clearly demonstrated that alprazolam can inhibit the T-cell proliferation in response to Con A but not to IL2. Alprazolam also reduced the production of IL2 by splenic T-cells, but did not alter the expression of IL2R on Con A-induced T-blast cells. Furthermore, the results also showed that (a) alprazolam did not inhibit the proliferative response of splenic T-cells to a combination of phorbol 12-myristate-13-acetate (PMA) and ionomycin, and (b) the addition of exogenous IL2 reversed the inhibitory effect of alprazolam on T-cell proliferation. Finally, the addition of alprazolam produced a time-dependent inhibiting effect on T-cell proliferation. However, this inhibitory effect of alprazolam was abolished when the drug was added to the cultures of competent cells that fully expressed IL2R. Taken together, these results suggest that alprazolam inhibits murine T-cell proliferation by affecting the mitogenic receptor-mediated events (initiation) rather than the IL2R-mediated events (progression) of ligand-activated T-cells through the cell cycle.

Alprazolam↗

PubMed1992

Prenatal exposure to alcohol enhances thymocyte mitogenic responses postnatally.

Previous studies have shown altered cell-mediated immune responses in animals prenatally exposed to ethanol. The present study was designed to determine the ontogeny of proliferative responses of thymocytes postnatally following prenatal exposure to ethanol. Thymocytes obtained from 44-day old Sprague-Dawley male rats exposed to 5% (w/v) ethanol during the last two weeks of gestation had a significantly greater response to mitogenic stimulation by concanavalin A (Con A, 5.0 micrograms/ml) than controls. A similar trend was observed in rats at postnatal days 30 and 72, but not at day 16. Con A-conditioned thymoblasts from day-44 fetal alcohol-exposed animals were less responsive to further activation by a crude Con A supernatant than controls, but this response normalized by day 72. These findings reveal that the effects of ethanol exposure in utero in male rats include alterations in the development of thymoproliferative responses to mitogen which persist through the peripubertal period and normalize in part by young adulthood.

Animals↗

PubMed1992

Mechanism of ethanol-mediated immunosuppression in mice: ethanol suppresses T-cell proliferation without affecting IL2 production and IL2 receptor expression.

The effect of extended ethanol consumption in young C57BL/6 mice on T-cell proliferation was studied. Splenic cells of young mice (3-4 months old), fed with one of three different liquid diets (5% ethanol, maltose-substitute, or standard liquid diet) for 28-38 days were cultured with plant lectins to assess T-cell proliferation and IL2 production. Expression of T-cell subset markers (CD4+/CD8+) was also determined. Then, Con A-activated T blast cells were assessed for their ability to express IL2 receptor (IL2R) and to respond to IL2. Finally, the proliferative response of splenic cells to PMA/ionomycin was assessed. The results showed that both lectin- and PMA/ionomycin-induced mitogenesis and IL2-dependent proliferation of T-cells from ethanol diet-fed mice were diminished as compared with that of maltose-substitute diet or standard liquid diet. However, the ability of T-cells from ethanol diet-fed mice to produce IL2 and to express IL2 R or CD4+/CD8+ subset markers was not affected. Furthermore, the magnitude of ethanol-mediated suppression of T-cell proliferation induced by PMA/ionomycin was comparable with that induced by Con A. These results taken together indicate that ethanol suppresses T-cell proliferation by interfering with events following the IL2-IL2R interaction. Therefore, it is likely that ethanol inhibits murine T-cell proliferation by selectively affecting the progression (IL2R-mediated events) rather than the initiation (mitogenic receptor-mediated events) of the cell cycle.

Animals↗

PubMed1992

Characterization of Staphylococcus aureus-platelet binding by quantitative flow cytometric analysis.

Quantitative analyses of Staphylococcus aureus binding to platelets were done using flow cytometry after bacterial exposure to the following treatments: proteases (trypsin, protease K), antibiotics (oxacillin, gentamicin), surface carbohydrate modifiers (sodium periodate, anticapsular antibody), or platelet microbicidal protein. In separate studies, platelets were exposed to a monoclonal antibody to their Fc receptor (Fc gamma RII) before binding was quantified. The percentage of bacteria bound to platelets varied significantly among strains (22.1% +/- 3.8% to 76.4 +/- 3.2%). For all isolates, binding to platelets was rapid, saturable, and reversible, suggesting a receptor-ligand interaction. The following modifiers significantly reduced binding: platelet microbicidal protein (by 32.1% +/- 5.2%; P less than .001), homologous (but not heterologous) anticapsular antibody (by 17.7% +/- 1.9%; P less than .05), sodium periodate (by 36.3% +/- 4.3%; P less than .005), and anti-platelet Fc monoclonal antibody (by 41.5% +/- 4.4%; P less than .002). Collectively, these data suggest that the mechanism(s) involved in S. aureus-platelet binding are complex and multimodal, involving carbohydrate-rich and platelet microbicidal protein-susceptible S. aureus surface ligands as well as the platelet Fc receptor.

Animals↗

PubMed1992

Effect of impaired renal function on the pharmacokinetics of coadministered cefoperazone and sulbactam.

The pharmacokinetics of cefoperazone 2 g combined with sulbactam 1 g after a single dose administered intravenously were evaluated in 24 subjects with normal and impaired renal function. Subjects were categorized into four groups based on endogenous creatinine clearance Clcr. Patients in groups 1, 2 and 3 had ClcrS of greater than 60, 31 to 60, and 10 to 30 mL/min/1.73 m2, respectively. Patients in group 4 required maintenance haemodialysis and were assumed to have Clcr less than 10 mL/min/1.73 m2. Pharmacokinetic parameters were determined by noncompartmental methods. No significant differences (P greater than 0.05) in mean peak serum cefoperazone-sulbactam concentrations for group 1 (208.4/29.0 mg/L), group 2 (199.0/34.1 mg/L), group 3 (163.2/35.0 mg/L), and group 4 (234.0/66.0 mg/L) were noted. Correlations between both total serum (r = 0.58) and renal (r = 0.35) clearance and creatinine clearances were negative for cefoperazone, although both were shown to decline with diminished renal function. Correlations between serum (r = 0.85) and renal (r = 0.72) clearances and creatinine clearance for sulbactam were, on the other hand, both positive and declined in a linear fashion. No significant differences in steady state volumes of distribution were noted for either cefoperazone (P = 0.53) or sulbactam (P = 0.85) amongst the four groups. After 24 h, urinary recovery was also comparable for both cefoperazone (P = 0.64) and sulbactam (P = 0.85) amongst the four groups. The concentrations of cefoperazone and sulbactam remained at or above the MICs (16/8 mg/L) for common bacterial pathogens for 2.5, 3, 7 and 14 h in groups 1, 2, 3 and 4, respectively.

Adolescent↗

PubMed1992

The equivalency of infrared tympanic membrane thermometry with standard thermometry in nursing home residents.

OBJECTIVE: To compare the equivalence of infrared tympanic membrane (TM) measure of body temperature with standard electronic oral (PO) and rectal (R) measures in a nursing home population. DESIGN: Randomized repeated-measurement design. METHODS: For the study, 82 randomly selected residents (mean age 79 +/- 10 years) of the Nursing Home Care Unit of the VAMC West Los Angeles had PO, R, and TM temperatures measured before arising (6-8 am). An otoscopic exam and the age, sex, presence of neurologic disease, and compliance with thermometry was noted. Also, repeated measures of PO and TM temperatures were performed three times to assess variability. The Pearson's correlation coefficient was determined for PO versus R and for TM versus R temperatures. Stepwise regression analysis was performed with the dependent variable of R temperature and the independent variables of the mean TM temperature, age, sex, presence of neurologic disease, position of the resident, and extent of ear canal occlusion. RESULTS: The correlation of TM versus R (r = .39, P = .004) was better, though not significantly, than of PO versus R (r = .28, P = .04). TM had less variability than PO (pooled standard deviation .38 vs .45 degrees F, respectively) and TM was implemented successfully more often than PO or R (96% vs 81% vs 81%). CONCLUSION: Therefore, TM was at least equivalent or better than PO measures of temperature in this population. The efficacy of fever detection and the use and durability of long-term use by nursing staff needs to be studied.

Aged↗

PubMed1992

Platelet microbicidal protein enhances antibiotic-induced killing of and postantibiotic effect in Staphylococcus aureus.

The interaction of bacteria with platelets at the cardiac valve surface represents a critical event in the induction of infective endocarditis. Platelets are thought to modulate induction or propagation of endocarditis via secretion of alpha-granule-derived platelet microbicidal protein (PMP) (a low-molecular-mass, cationic, heat-stable protein distinct from lysozyme). We studied representative PMP-susceptible and PMP-resistant Staphylococcus aureus isolates to determine their in vitro bacteriostatic and bactericidal susceptibilities to combinations of PMP plus antistaphylococcal antibiotics. PMP plus oxacillin exerted a synergistic bactericidal effect, in contrast to either agent alone, regardless of the intrinsic PMP susceptibility of the isolate tested. Exposure of S. aureus to PMP alone resulted in residual postexposure growth-inhibitory effects lasting from 0.9 to 1.8 h. Sequential exposure of S. aureus isolates to PMP for 30 min followed by exposure to either oxacillin or vancomycin (each at 10x the MIC for 120 min) resulted in a significant extension of the postantibiotic-effect duration compared with antibiotic exposure alone (P less than or equal to 0.05). Collectively, these findings indicate that PMP both enhances antibiotic-induced killing of S. aureus and increases the postantibiotic-effect duration in S. aureus.

Animals↗

PubMed1992

Partial characterization and staphylocidal activity of thrombin-induced platelet microbicidal protein.

Thrombin-induced platelet microbicidal protein (PMP) is considered to play an important role in preventing an important role in preventing streptococcal endocarditis. However, the structural features and functions of PMPs have not been well characterized, and their antibacterial spectra against other common endocarditis pathogens, such as the staphylococci, are not known. Thrombin stimulation of washed rabbit platelets (10(8)/ml) yielded a PMP-rich preparation with a specific activity of approximately 25 U/mg of protein as determined by Bacillus subtilis bioassay. Twenty-eight clinical and laboratory Staphylococcus aureus isolates, exposed to a standardized PMP preparation (100 U/ml for 2 h at 37 degrees C), exhibited a Poisson-distributed heterogeneity to the bactericidal action of PMP, with approximately one-third designated as PMP resistant. Gel filtration chromatography (Sephadex G-50) identified the bioactive moiety within PMP preparations to be in the major protein elution peak; sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) presumptively identified PMP as a low-molecular-weight (MW) (8,500) protein present only in such bioactive protein peaks. Both the bioactivity of PMP preparations and the low-MW protein band were removable by specific anionic membranes (e.g., cellulose-acetate/nitrate), as well as by a variety of anionic resins, further corroborating the suspected cationic charge of PMP. In addition, both PMP bioactivity and the low-MW protein band were recoverable by 1.5 M NaCl elution of the anionic membrane filters post-PMP adsorptive removal. Adsorption of bioactive PMP preparations by highly PMP-susceptible B. subtilis (10(8) CFU/ml, 30 min) resulted in a near-complete loss of residual bioactivity; in contrast, adsorption of bioactive PMP preparations with less PMP-susceptible S. aureus strains failed to reduce bioactivity. Significant lysozyme contamination of PMP-rich preparations was ruled out by determination of differences between bioactive PMP preparations and exogenous lysozyme as regards (i) relative heat stabilities; (ii) differential bactericidal activity versus B. subtilis and Micrococcus luteus; and (iii) SDS-PAGE protein profiles. These data show that the bioactive PMP protein moiety is of low MW, is heat stable, is probably cationic (similar to leukocyte-derived defensins), and possesses potent bactericidal activity against a significant percentage of S. aureus isolates.

Animals↗

PubMed1992

Staphylococcus aureus susceptibility to thrombin-induced platelet microbicidal protein is independent of platelet adherence and aggregation in vitro.

Bacterium-platelet interactions at the cardiac valve surface represent an important initial step in the induction of infective endocarditis (IE). This cell-cell interaction may play either a protagonistic role in the induction of IE via bacterial adherence to and aggregation of platelets or an antagonistic role via secretion of platelet-derived microbicidal molecules. We examined the spectrum and interrelationship of three aspects of the interaction of 20 clinical Staphylococcus aureus isolates with rabbit platelets in vitro: (i) S. aureus adherence to platelets; (ii) S. aureus-induced platelet aggregation; and (iii) S. aureus resistance to the action of thrombin-induced platelet microbicidal protein (PMP; low-molecular-weight cationic peptides contained in alpha granules). Among the 20 S. aureus isolates (11 bacteremia, 9 endocarditis), there was a heterogeneous distribution profile for each of the bacterium-platelet interaction parameters studied. For S. aureus-platelet adherence and S. aureus-induced platelet aggregation, 3 of 20 and 7 of 20 isolates tested were considered highly active for each respective parameter; 5 of 20 staphylococcal strains were deemed resistant to the bactericidal action of PMP. In addition, more endocarditis isolates (45%) were PMP resistant than strains from patients without endocarditis (19%). When analyzed concomitantly, there was a significant, positive correlation between S. aureus-platelet adherence and S. aureus-induced platelet aggregation among isolates (P = 0.003; r = 0.78). In contrast, there were no statistically significant relationships between either platelet adherence or aggregation and PMP resistance among these 20 S. aureus isolates. These data suggest that platelet adherence and aggregation are related abilities of S. aureus, while resistance to thrombin-induced PMP is an independent phenotypic characteristic and potential virulence factor.

Animals↗

PubMed1992

Infections in elderly persons. An altered clinical presentation.

The high prevalence, morbidity, and mortality of infectious diseases in the geriatric population mandates that clinicians caring for older patients become better acquainted and familiar with the special and unique characteristics and features of this common clinical problem. Only through such awareness and understanding will clinical outcomes, functional capacity, and quality of life be improved in the elderly population.

Aged↗

PubMed1991

Immunotoxicity of alcohol in young and old mice. II. Impaired T cell proliferation and T cell-dependent antibody responses of young and old mice fed ethanol-containing liquid diet.

The effect of extended ethanol consumption of young and old BALB/c mice on the proliferative response to Concanavalin A (Con A) and T cell-dependent antibody response of their spleen cells to sheep red blood cell (RBC) stimulation was determined. Splenic cells of young (3 months) and old (25 months) BALB/c mice, fed with one of three different diets (ethanol, maltose-substitute and standard mouse chow), were first cultured with Con A to assess T cell proliferation and production of interleukin 2 (IL2). Then, Con A-activated T blast cells from young and old mice were assessed for their proliferative responding capacity to exogenous human recombinant IL2 and crude rat IL2 supernatant. Finally, splenic cells of young and old mice were assessed for their ability to generate plaque-forming cells in response to sheep RBC. The results revealed that both T cell mitogenesis and IL2-dependent proliferation of T blast cells from young and old ethanol diet-fed mice were remarkably diminished as compared to that of young and old maltose-substituted diet (isocaloric control) fed mice, respectively. The ability of T cells from both young and old ethanol diet-fed mice to produce IL2, however, was not affected. Finally, the ability of young and old ethanol diet-fed mice to mount a primary antibody response to SRBC was also significantly reduced. These results taken together demonstrate for the first time that both T cell proliferative activity and T cell-dependent antibody response of young and old ethanol diet-fed mice are impaired; however, with respect to age, a differential effect of immunosuppression of ethanol was not noted.

Aging↗

PubMed1991

Suppressive effects of alprazolam on the immune response of mice.

The purpose of this study was to examine the effects of alprazolam on the response of murine immune cells. Splenic cells of young BALB/c mice were first cultured with an optimum dose of various mitogens in the presence or absence of varying doses of alprazolam to assess effects of alprazolam on concanavalin A (Con A)-induced T-cell proliferation, bacterial lipopolysaccharide (LPS)-induced B-cell proliferation, and production of interleukin 2 (IL2). Then, peritoneal adherent cells (macrophages) from young BALB/c mice were cultured with an optimum dose of LPS in the presence or absence of alprazolam to assess the effects of alprazolam on the ability of peritoneal adherent cells to produce interleukin 1 (IL1) and tumor necrosis factor (TNF). The results of this study clearly demonstrated that alprazolam is a potent immunosuppressive agent that can inhibit the proliferative responses of both B- and T-cells to LPS and Con A, respectively. It also can reduce production of IL2 by splenic T-cells and production of both IL1 and TNF by peritoneal macrophages. Furthermore, it was also shown that (a) the magnitude of suppression of T-cell proliferation and of IL2 production occurs in a dose-dependent manner and (b) B-cells are more vulnerable than T-cells to the effect of alprazolam.

Alprazolam↗

PubMed1991

Changes with age in the proliferative response of splenic T cells from rats exposed to ethanol in utero.

The fetal alcohol syndrome is associated with altered immunity. Several laboratories have confirmed that rodents exposed to ethanol in utero demonstrate both diminished proliferative responses of T cells to mitogens and diminished proliferative responses of T-blast cells to human recombinant interleukin 2 (rIL2). We examined the developmental time course of these altered immune responses by testing the immune function of in utero ethanol-exposed rats at various ages. We found that while diminished splenic T cell proliferative responses could not be detected at 2 weeks, they were present at 6 weeks after birth and suppression was maximal at 6 weeks and 3 months. Thereafter, at 5 and 7 months, the altered immune responses gradually declined and normalized at 8 months of age. Thus, both altered T cell mitogenesis and the blunted IL2-induced proliferative response of T-blast cells could serve as biomarkers of fetal exposure to ethanol.

Age Factors↗

PubMed1991

Fever response in elderly nursing home residents: are the older truly colder?

OBJECTIVE: To test the hypothesis that many nursing home residents with an apparently blunted fever response (maximum temperature less than 101 degrees F) may actually have a significant change in temperature (delta T greater than or equal to 2.4 degrees F) which is not recognized because of a low baseline temperature. DESIGN: Retrospective chart review for cases of infection that met specific criteria and for chart-recorded baseline and infection temperatures. Chart-recorded baseline temperatures were prospectively compared with re-measurement of morning temperatures. SETTING: Nursing Home Care Unit of the VAMC West Los Angeles. PATIENTS: Random review of 40 residents' charts resulted in the detection of 69 infections among 26 residents over a 20-month period. Fifty randomly selected residents prospectively underwent comparison of chart-determined and actual re-measurement of baseline temperatures. RESULTS: In 50 randomly selected residents, the mean oral baseline temperature of 97.4 +/- 0.2 (degrees F +/- SEM) closely approximated the mean nurse-recorded measures in the charts (97.6 +/- 0.1). Chart review detected 69 infections among 26 residents, with 53 episodes having a temperature recorded during the infection. The mean maximum temperature (Tmax) during an infection was 101.3 +/- 0.3 (degrees F +/- SEM) but 47% (25/53) of the episodes had a "blunted" fever response (Tmax less than 101 degrees F). Of the 25 "blunted" fevers (Tmax less than 101 degrees F), about one-fourth demonstrated an adequate change in temperature from baseline (delta T greater than or equal to 2.4 degrees F) but failed to reach 101 degrees F because of a low baseline. Most infections (89%) had a Tmax greater than 99 degrees F. CONCLUSION: Establishing a nursing home patient's basal temperature and monitoring for changes in temperature (delta T greater than 2.4 degrees F) and/or lowering the threshold for recognition of fevers (to 99 degrees or 100 degrees F) in nursing home residents with a change in function should assist in early recognition of infections.

Aged↗

PubMed1991

Functional role of mucoid exopolysaccharide (alginate) in antibiotic-induced and polymorphonuclear leukocyte-mediated killing of Pseudomonas aeruginosa.

We evaluated in vitro the functional role of mucoid exopolysaccharide (MEP) of Pseudomonas aeruginosa in blocking antibiotic-induced and polymorphonuclear leukocyte (PMN)-mediated pseudomonal killing. The serum-resistant P. aeruginosa isolates used were mucoid strain 144MR and its nonmucoid revertant, strain 144NM. By timed kill curves, early bacterial effects of amikacin against mucoid strain 144MR were substantially less than those observed with nonmucoid strain 144NM; this effect was reversible with enzymatic hydrolysis of MEP of strain 144MR by alginase. Also, early tobramycin uptake (15 to 30 min) by mucoid 144MR cells was less than that seen with nonmucoid strain 144NM; pretreatment of 144MR cells with alginase substantially enhanced early tobramycin uptake compared with untreated 144MR cells (P = 0.08). In strain 144NM (but not in strain 114MR) there was a notable postantibiotic leukocidal enhancement effect manifested by increased nonopsonic killing following brief exposure of these cells to supra-MIC amikacin; pretreatment of strain 144MR with alginase rendered these cells more susceptible to amikacin-induced postantibiotic leukocidal enhancement. Similarly, direct PMN-mediated nonopsonic killing of mucoid strain 144MR was significantly less than that observed with strain 144NM (P less than 0.05); pretreatment of 144MR cells with alginase rendered this strain equal to strain 144NM in susceptibility to nonopsonic killing. In addition, exogenous sodium alginate or extracted MEP of strain 144MR interfered with effective nonopsonic killing of strain 144NM by PMNs. Studies also indicated that mucoid strain 144MR was phagocytosed significantly less well than its nonmucoid mate (P less than 0.00001), an effect reversed by pretreatment of the mucoid cells with alginase. These data confirm that P. aeruginosa MEPs functionally decrease the uptake and early bactericidal effect of aminoglycosides in vitro and interfere with effective PMN-mediated nonopsonic phagocytosis and killing of mucoid strains.

Alginates↗

PubMed1991

Pneumonia in the elderly: empiric antimicrobial therapy.

Pneumonia, the leading cause of death due to infectious disease in the elderly, can be difficult to diagnose in this age group because clinical signs and symptoms are often muted. Without a definitive isolate, the physician must institute empiric therapy with broad-spectrum antibiotics according to the patient's condition and the setting in which the pneumonia developed. The cephalosporins, because of their safety profiles, are often used alone or in combination with other drugs to achieve broad antimicrobial coverage in elderly patients with pneumonia. In general, elderly patients with pneumonia should be hospitalized, although nursing home residents may be managed in the nursing home if adequate staff and resources are available.

Aged↗

PubMed1990

Immunotoxicity of alcohol in young and old mice. I. In vitro suppressive effects of ethanol on the activities of T and B immune cells of aging mice.

A murine aging model was employed to assess effects of ethanol exposure on the T-cell proliferative response to mitogenic stimulation and on the T cell-dependent primary antibody response to sheep red blood cells (RBC) in vitro. Splenic cells from young (3-5 months) and old (28-32 months) BALB/c mice were first assessed for their ability to produce interleukin (IL) 2 and proliferate in response to mitogenic stimulation in the presence of various doses of ethanol. Then, splenic T blast cells from young and old mice, generated by Con A-activation, were assessed for their IL2-dependent proliferative capacity in the presence of various doses of ethanol. Finally, splenic cells of young and old mice were assessed for their ability to generate plaque-forming cells (PFC) in response to sheep RBC in the presence of various doses of ethanol. The results revealed that ethanol has a much greater suppressive effect on old than young splenic T cells (10-15 times), as judged by their ability to proliferate in response to mitogenic stimulation. However, the magnitude of the difference in the suppressive effect is less when the cells are cycling (2 times). Furthermore, ethanol had only a minimal suppressive effect on IL2 production by T cells of both young and old mice, even at the concentration of 100 mM. These findings would suggest that the ethanol-mediated suppression of T cell proliferation of both young and old mice is more likely due to an impairment of metabolic event(s) associated with or subsequent to the interaction of IL2 and IL2 receptor leading to cellular replication.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1990

Clinically inapparent (asymptomatic) bacteriuria in ambulatory elderly men: epidemiological, clinical, and microbiological findings.

In a prospective longitudinal study, ambulatory elderly men were followed from 1 to 4.5 years to gain insight into the prevalence rates, clinical characteristics, and patterns of clinically inapparent (asymptomatic) bacteriuria (CIB). The prevalence of CIB was 12% (29/238) and increases with age. Unlike the gram-negative organisms that cause overt urinary tract infection in this age group, gram-positive organisms dominated the CIB group. Both the CIB and abacteriuric patients have multiple chronic medical conditions and are indistinguishable on that basis. Twenty-nine elderly men with bacteriuria and 105 abacteriuric subjects were followed with serial urine cultures. During the study period the bacteriuric subjects exhibited spontaneous temporary or permanent resolution (76%, 22/29), intermittency (21%, 6/29), and probable bacterial persistence (38%, 11/29). No consistent pattern of bacteriuria was evident. Therefore, antimicrobial therapy is not warranted in the treatment of asymptomatic or clinically inapparent bacteriuria in ambulatory elderly men.

Age Factors↗