Campylobacter jejuni infection in broiler chickens.

Day-old, straight-run broiler chickens were procured from a hatchery located in the Pacific Northwest. The chickens were subdivided individually into nine groups of 20 chickens. The chickens were tagged, housed in isolation chambers on wire, fed commercial broiler feed, and given water ad libitum. Three isolates of Campylobacter jejuni of poultry origin and one of human origin were tested in this study. Various C. jejuni cultures were inoculated into 9-day-old chickens by crop gavage. Four groups of 20 chickens were inoculated at a dose level of 0.5 ml of 1 x 10(2) colony-forming units (CFU)/ml. The other four groups were inoculated with 0.5 ml of 1 X 10(4) CFU/ml. One group of 20 chickens was kept as an uninoculated control group. Four randomly selected chickens from each of the inoculated and uninoculated groups were necropsied at 5, 12, and 19 days postinoculation (DPI). The C. jejuni was cultured and enumerated from a composite of the upper and midintestine and the cecum. Body weights of all chicken groups at 7 days of age and at 5, 12, and 19 DPI were measured and statistically analyzed. No significant differences were present in the mean body weights (MBWs) of 7-day-old, 5 DPI, and 12 DPI male and female broiler chickens inoculated with C. jejuni at both dose levels compared with uninoculated controls. Differences in MBWs of the male and female broilers at 19 DPI were observed in some of the groups. Results of the C. jejuni culture enumeration mean (CEM) of composite intestine samples at 5 DPI from all inoculated chicken groups, irrespective of the dose level, ranged from (2.5 +/- 5.0) x 10(2) to (2.8 +/- 4.8) x 10(5) CFU/g (mean +/- SD). Results of cecum C. jejuni CEM at 5 DPI inoculated at both dose levels ranged from (2.5 +/- 5.0) x 10(6) to (1 +/- 0.0) x 10(7) CFU/g in all treatment groups irrespective of the dose level. CEM results from the composite intestine samples at 12 and 19 DPI increased by 1 log unit, or sometimes more. Results of cecum C. jejuni CEM at 5 DPI inoculated at both dose levels ranged from (2.5 +/- 5.0) x 10(6) to (1 +/- 0.0) x 10(7) CFU/g in all treatment groups irrespective of the dose level. Increases of 2-5 log units in C. jejuni CEM was present in chicken groups inoculated with 1 X 10(2) CFU of C. jejuni, and a 2- to 3-log increase was present in groups inoculated with a higher dose level of C. jejuni at 12 DPI. The results of C. jejuni CEM from cecal samples at 19 DPI were similar to chicken groups at 12 DPI. Campylobacterjejuni was not isolated from the uninoculated control chickens at 5, 12, and 19 DPI. Clinical signs of illness or gross pathologic lesions were not present in any of the chicken groups during this study. No lesions were present on histopathologic evaluations in C. jejuni-inoculated chickens or uninoculated control chickens.

Results of salmonella isolation from poultry products, poultry, poultry environment, and other characteristics.

Five hundred sixty-nine Salmonella were isolated out of 4745 samples from poultry products, poultry, and poultry environment in 1999 and 2000 from the Pacific northwest. These Salmonella were identified to their exact source, and some were serogrouped, serotyped, phage typed, and tested for antibiotic sensitivity. Food product samples tested included rinse water of spent hens and broilers and chicken ground meat. Poultry environment samples were hatchery fluff from the hatcheries where eggs of grandparent broiler breeders or parent broiler breeder eggs were hatched and drag swabs from poultry houses. Diagnostic samples were of liver or yolk sac contents collected at necropsy from the young chicks received in the laboratory. Of these samples tested, 569 were Salmonella positive (11.99%). Ninety-two Salmonella were serogrouped with polyvalent somatic antisera A-I and the polymerase chain reaction. Somatic serogroups B and C comprised 95.25% of all the Salmonella. Out of a total of 569 positive samples, 97 isolates of Salmonella were serotyped. A total of 16 serotypes and an unnamed Salmonella belonging to serogroup C1 were identified. The Salmonella serotypes were heidelberg (25.77%); kentucky (21.64%); montevideo (11.34%); hadar and enteritidis (5.15% each); infantis, typhimurium, ohio, and thompson (4.12% each); mbandaka and cerro (3.09% each); senftenberg (2.06%); berta, istanbul, indiana, and saintpaul (1.03% each); and an unnamed monomorphic Salmonella (2.06%). Ninety-two Salmonella were tested for drug sensitivity with nine different antimicrobials. All of the 92 Salmonella were resistant to erythromycin, lincomycin, and penicillin except one sample (S. berta), which was moderately sensitive to penicillin. All of the tested Salmonella were susceptible to sarafloxacin and ceftiofur. The percentages of Salmonella susceptible to sulfamethoxazole-trimethoprim, gentamicin, triple sulfa, and tetracycline were 97.83%, 92.39%, 86.96%, and 82.61%, respectively.

Effects of methylprednisolone on intracellular bacterial growth.

Clinical studies have shown positive associations among sustained and intense inflammatory responses and the incidence of bacterial infections. Patients presenting with acute respiratory distress syndrome (ARDS) and high levels of proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and IL-6, have increased risk for developing nosocomial infections attributable to organisms such as Staphylococcus aureus, Pseudomonas aeruginosa, and Acinetobacter spp., compared to those patients with lower levels. Our previous in vitro studies have demonstrated that these bacterial strains exhibit enhanced growth extracellularly when supplemented with high concentrations of pure recombinant TNF-alpha, IL-1 beta, or IL-6. In addition, we have shown that the intracellular milieu of phagocytic cells that are exposed to supraoptimal concentrations of TNF-alpha, IL-1 beta, and IL-6 or lipopolysaccharide (LPS) favors survival and replication of ingested bacteria. Therefore, we hypothesized that under conditions of intense inflammation the host's micromilieu favors bacterial infections by exposing phagocytic cells to protracted high levels of inflammatory cytokines. Our clinical studies have shown that methylprednisolone is capable of reducing the levels of TNF-alpha, IL-1 beta, and IL-6 in ARDS patients. Hence, we designed a series of in vitro experiments to test whether human monocytic cells (U937 cells) that are activated with high concentrations of LPS, which upregulate the release of proinflammatory cytokines from these phagocytic cells, would effectively kill or restrict bacterial survival and replication after exposure to methylprednisolone. Fresh isolates of S. aureus, P. aeruginosa, and Acinetobacter were used in our studies. Our results indicate that, compared with the control, stimulation of U937 cells with 100-ng/ml, 1.0-microg/ml, 5.0-microg/ml, or 10.0-microg/ml concentrations of LPS enhanced the intracellular survival and replication of all three species of bacteria significantly (for all, P = 0.0001). Stimulation with < or =10.0 ng of LPS generally resulted in efficient killing of the ingested bacteria. Interestingly, when exposed to graded concentrations of methylprednisolone, U937 cells that had been stimulated with 10.0 microg of LPS were able to suppress bacterial replication efficiently in a concentration-dependent manner. Significant reduction in numbers of CFU was observed at > or =150 microg of methylprednisolone per ml (P values were 0.032, 0.008, and 0.009 for S. aureus, P. aeruginosa, and Acinetobacter, respectively). We have also shown that steady-state mRNA levels of TNF-alpha, IL-1 beta, and IL-6 in LPS-activated cells were reduced by treatment of such cells with methylprednisolone, in a concentration-dependent manner. The effective dose of methylprednisolone was 175 mg, a value that appeared to be independent of priming level of LPS and type of mRNA. We therefore postulate that a U-shaped relationship exists between the level of expression of TNF-alpha, IL-1 beta, and IL-6 within the phagocytic cells and their abilities to suppress active survival and replication of phagocytized bacteria.

Pathogenicity of environmental origin Salmonellas in specific pathogen-free chicks.

Two hundred sixty 1-d-old specific pathogen-free (SPF), Single Comb White Leghorn chicks were used in this study to determine pathology caused by Salmonella enteritidis (SE) isolated from a poultry environment. The chicks were subdivided into 10 equal groups of 26 chicks each. Eight groups of chicks were inoculated individually with 0.5 mL of brain heart infusion broth culture containing 1 x 10(6) cfu of SE phage type (PT) -8 (1, 2, 3), SE PT5 A (1, 2), or SE PT4 (Ch-env-CA, chicken-CA, and human) by crop gavage. One group of 26 chicks were inoculated with 1 x 10(6) cfu of Salmonella pullorum per bird by crop gavage. Another group of 26 chicks were kept as an uninoculated control group. All the chicks were observed daily for clinical signs and mortality. Salmonella was reisolated from different organs at 7, 14, 21, and 28 postinoculation (DPI). All of the chicks were weighed individually at each interval. Two chicks at random from each group were euthanised and necropsied at each DPI for gross pathology. Selected tissues were examined for histopathological changes at 7 and 14 DPI. Dead chicks were examined for gross and histopathological lesions. Mortality rates were 30.7, 15.3, and 7.6% in the groups inoculated with S. pullorum, SE PT5A, and SE PT4 (chicken-CA), respectively. No mortality or clinical sign were observed in other treatment groups or in uninoculated control groups. Cecal pouches were found to be the ideal organ for reisolation of Salmlonella at acute or chronic infection compared with other organs. Mean body weights were reduced to 1.8 to 12.6% in inoculated groups compared with the uninoculated control group. The consistent gross and hispathological lesions were of peritonitis, perihepatitis, yolk sac infection, and enteritis. Subclinical Salmlonella infection identified in this study resulted in reduced body weights of inoculated birds compared with uninoculated controls.

Enhanced extracellular growth of Staphylococcus aureus in the presence of selected linear peptide fragments of human interleukin (IL)-1beta and IL-1 receptor antagonist.

Replication of Staphylococcus aureus is significantly enhanced in the presence of recombinant interleukin (IL)-1beta. In this study, specific binding of IL-1beta to the surface of S. aureus significantly increased growth of S. aureus in the presence of IL-1beta and IL-1ra in a concentration-dependent manner. Although IL-1ra enhanced the growth of S. aureus, there was a significant reduction in IL-1beta-mediated growth enhancement of S. aureus when 25-fold excess amounts of IL-1ra (in comparison with the IL-1beta concentration) were present in the culture medium. Thus, IL-1beta may influence the growth of S. aureus through a receptor-mediated event. By using 5 linear peptides spanning limited regions of IL-1beta, the growth-promoting regions were localized to amino acid residues 118-147 and 208-240. These results build on the newly evolved concept of direct interactions between the soluble mediators of inflammation and infectious agents.

Pathogenicity of different serogroups of avian salmonellae in specific-pathogen-free chickens.

The pathogenicity of one isolate of Salmonella typhimurium, four isolates of Salmonella heidelberg, three isolates of Salmonella kentucky, two isolates of Salmonella montevideo, one isolate of Salmonella hadar, and two isolates of Salmonella enteritidis (SE), one belonging to phage type (PT)13a and the other to PT34, was investigated in specific-pathogen-free chicks. Three hundred eighty-four chicks were separated into 16 equal groups of 24 chicks. Thirteen groups were inoculated individually with 0.5 ml of broth culture containing 1 x 10(7) colony-forming units (CFU) of either S. typhimurium (one source), S. heidelberg (four sources), S. montevideo (two sources), S. hadar (one source), S. kentucky (three sources), SE PT 13a (one source) or SE PT 34 (one source) by crop gavage. Two groups of 24 chicks were inoculated in the same way with 1 x 10(7) CFU of SE PT4 (chicken-CA) and Salmonella pullorum. Another group of 24 chicks was kept as an uninoculated control group. The chicks were observed daily for clinical signs and mortality. Isolation of salmonella was done from different organs at 7 and 28 days postinoculation (DPI). All the chicks were weighed individually at 7, 14, 21, and 28 DPI. Two chicks chosen at random from each group were euthanatized and necropsied at 7 and 14 DPI and all the remaining live chickens, at 28 DPI. Selected tissues were taken for histopathology at 7 and 14 DPI. Dead chicks were examined for gross lesions and tissues were collected for histopathology. Chicks inoculated with S. pullorum had the highest mortality (66.66%), followed by S. typhimurium (33.33%). Chicks inoculated with S. heidelberg (00-1105-2) and SE PT4 (chicken-CA) had 12.5% mortality and 8.3% mortality, respectively, with SE PT 13a. Ceca were 100% positive for salmonellae at acute or chronic infection compared with other organs. Mean body weight reduction ranged from 0.67% (inoculated with S. kentucky 00-926-2) to 33.23% (inoculated with S. typhimurium 00-372) in the inoculated groups at different weeks compared with uninoculated controls. Gross and microscopic lesions included peritonitis, perihepatitis, yolk sac infection, typhilitis, pneumonia, and enteritis in some groups, especially those inoculated with S. typhimurium, S. heidelberg (00-1 105-2), SE PT4 (chicken-CA), and S. pullorum.

Pathogenicity of Salmonella enteritidis phage types 4, 8 and 23 in specific pathogen free chicks.

The pathogenicity of two isolates of Salmonella enterica serovar Enteritidis (SE) phage type (PT) 4, three of PT8 and one of PT23 was investigated in groups of 1-day-old specific pathogen free White Leghorn chicks. Two groups were crop gavaged with each culture but at two different doses. Two additional groups were given Salmonella enterica serovar Pullorum (SP) at similar doses and one further group served as uninoculated controls. Body weights were recorded at 14, 21, and 28 days postinoculation (d.p.i), and mortality was monitored throughout. In most treatment groups, the average body weights were significantly lower than the controls. Birds inoculated with SP had the highest mortality followed by those given SE PT4 of human or chicken origin. At 14 and 21 d.p.i., four chicks from each group were killed and examined for gross lesions. Selected tissues were collected for histopathology and cultured for bacteria. Dead birds had fibrinous exudate in the pericardium and also, in a few, on the liver capsule. They had enlarged livers, sometimes with congestion and white foci. At 7 d.p.i., several birds, especially those inoculated with SE PT4, had retained yolk sacs containing coagulated material. Microscopic lesions of pericarditis, myocarditis, hepatitis, splenitis, peritonitis and enteritis were present at 7 d.p.i. in most birds inoculated with SE, but was greatly variable at 14 d.p.i.. This study shows that 1-day-old SPF chicks are susceptible to various phage types of SE, with yolk-sac infection as the most prominent feature.

Cytokines IL-1beta, IL-6, and TNF-alpha enhance in vitro growth of bacteria.

We have previously reported that in acute respiratory distress syndrome (ARDS), nonsurvivors have persistent elevation in pulmonary and circulating proinflammatory cytokine levels over time and a high rate of nosocomial infections antemortem. In these patients, none of the proven or suspected nosocomial infections caused a transient or sustained increase in plasma proinflammatory cytokine levels above preinfection values. We hypothesized that cytokines secreted by the host during ARDS may favor the growth of bacteria. We conducted an in vitro study of the growth of three bacteria clinically relevant in nosocomial infections, evaluating their in vitro response to various concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. We found that all three bacterial species showed concentration-dependent growth enhancement when incubated with one or more tested cytokines and that blockade by specific neutralizing cytokine MoAb significantly inhibited cytokine-induced growth. When compared with control, the 6-h growth response (cfu/ml) was maximal with IL-1beta at 1,000 pg for Staphylococcus aureus (36 +/- 16 versus 377 +/- 16; p = 0.0001) and Acinetobacter spp. (317 +/- 1,147 versus 1,124 +/- 147; p = 0.002) and with IL-6 at 1,000 pg for Pseudomonas aeruginosa (99 +/- 50 versus 509 +/- 50; p = 0.009). The effects of cytokines were seen only with fresh isolates and were lost with passage in vitro on bacteriologic medium without added cytokines. In this study we provide additional evidence for a newly described pathogenetic mechanism for bacterial proliferation in the presence of exaggerated and protracted inflammation.

Academic managed care organizations and adverse selection under Medicaid managed care in Tennessee.

CONTEXT: Health plans competing in a managed care system may face serious financial consequences if they are disproportionately selected by enrollees with expensive health conditions. Academic medical centers (AMCs) have traditionally provided medical care for the sickest patients and may be at particularly high risk for adverse selection, but whether this occurs is not known. OBJECTIVE: To determine whether managed care organizations (MCOs) representing AMCs are adversely selected by Medicaid managed care (MMC) enrollees with expensive chronic health conditions. DESIGN AND SETTING: Observational study using state Medicaid claims data from all of 1994 and January to August 1995 for Tennessee's statewide MMC program (TennCare). PARTICIPANTS: All 12 capitated MCOs in Tennessee, which collectively provided services for 1.2 million Medicaid enrollees from January 1994 through August 1995 following the initiation of TennCare. MAIN OUTCOME MEASURES: Prevalence of 6 state-specified high-cost chronic conditions-acquired immunodeficiency syndrome (AIDS), coagulation defects, cystic fibrosis, pregnancy, prematurity, and organ transplantation-and 27 additional high-cost conditions compared by academic, statewide, and regional MCOs. RESULTS: The prevalence of state-specified high-cost chronic conditions was generally higher for academic MCOs compared with other MCOs. Specifically, prevalence of AIDS was 14.1 times higher in academic MCOs than in statewide MCOs; coagulation defects, 6.4 times higher; transplantations, 4.4; pregnancy, 3.3; cystic fibrosis, 2.4; and prevalence of prematurity was equivalent. Prevalence was higher for academic than for statewide MCOs for 22 of the additional 27 high-cost conditions considered and similar for the remaining 5 conditions. CONCLUSIONS: Our results suggest that academic MCOs in an MMC system are selected by a large percentage of the sickest patients. Adverse selection may present serious financial risks for AMCs participating in managed care.

Pathogenicity of Salmonella enteritidis phage types 4, 8, and 23 in broiler chicks.

Four hundred fifty day-old Hubbard broiler chicks were subdivided into 15 groups of 30 chicks each. Six groups of chicks received 0.5 ml of broth culture containing 5 x 10(6) colony-forming units (CFU) of Salmonella enteritidis (SE) phage types (PTs) 4, 8, and 23 by crop gavage. Similarly, six other groups received 0.5 ml containing 5 x 10(8) CFU of SE. One group was inoculated with 0.5 ml containing 5 x 10(6) CFU of Salmonella pullorum, and another group received 0.5 ml containing 5 x 10(8) CFU of S. pullorum. A group of 30 chicks were kept as uninoculated controls. Chicks were observed daily for clinical signs and mortality. All birds were weighed at 7, 14, and 21 days postinoculation 21 (DPI). Four chicks were randomly selected from each treatment group, euthanatized, and necropsied at 7 and 14 DPI. Gross lesions were recorded and selected tissues were collected for histopathology. The higher rates of illness and mortality were observed in chicks inoculated with 5 x 10(6) and 5 x 10(8) CFU of S. pullorum, followed by SE PT4 of human origin and SE PT4 of chicken origin. Moderate to high mortality was observed in chicks inoculated with the higher dose of SE isolates that belonged to PT8 and one SE of PT23. Variable mortality was evident in groups inoculated with the lower dose of salmonella. The most consistent gross and histopathologic changes, including fibrinous pericarditis and perihepatitis, were seen in the dead birds from various treatment groups. The lower mean body weights were present in all treatment groups compared with uninoculated controls. No illness or mortality was observed in uninoculated control groups.

Effects of cytokines and endotoxin on the intracellular growth of bacteria.

Patients with unresolving acute respiratory distress syndrome (ARDS) have persistently elevated levels of proinflammatory cytokines in the lungs and circulation and increased rates of bacterial infections. Phagocytic cells hyperactivated with lipopolysaccharide (LPS), which induces high levels of proinflammatory cytokines in monocytic cells, are inefficient in killing ingested bacteria despite having intact phagocytic activity. On the other hand, phagocytic cells that are activated with an analogue of LPS that does not induce the expression of proinflammatory cytokines effectively ingest and kill bacteria. We hypothesized that in the presence of high concentrations of proinflammatory cytokines, bacteria may adapt and utilize cytokines to their growth advantage. To test our hypothesis, we primed a human monocytic cell line (U937) with escalating concentrations of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-6 and with LPS. These cells were then exposed to fresh isolates of three common nosocomial pathogens: Staphylococcus aureus, Pseudomonas aeruginosa, and an Acinetobacter sp. In human monocytes primed with lower concentrations of proinflammatory cytokines (10 to 250 pg) or LPS (1 and 10 ng), intracellular bacterial growth decreased. However, when human monocytes were primed with higher concentrations of proinflammatory cytokines (1 to 10 ng) or LPS (1 to 10 micrograms), intracellular growth of the tested bacteria increased significantly (P <0.0001). These results were reproduced with peripheral blood monocytes obtained from normal healthy volunteers. The specificity of the cytokine activity was demonstrated by neutralizing the cytokines with specific antibodies. Our findings provide a possible mechanism to explain the frequent development of bacterial infections in patients with an intense and protracted inflammatory response.

Nosocomial pneumococcal infection: an outbreak.

When an outbreak of pneumococcal disease occurs an institution--be it a hospital, nursing home, day care center, or other facility--management includes treatment of affected cases and prevention of new cases. Patients and staff should be tested for nasopharyngeal carriage and their vaccination status ascertained. Antibiotic use should be reviewed, especially if the causative strain is resistant.

Oral staphylococcus in older subjects with rheumatoid arthritis.

OBJECTIVE: To determine if Staphylococcus aureus and Staphylococcus epidermidis, etiologic bacterial agents to late prosthetic joint infections (LPJI), are more prevalent in the oral flora of older individuals with rheumatoid arthritis (RA) than in an age and gender-matched nonarthritic control population (NA). DESIGN: Cultures were obtained from the nares, oropharynx, saliva, tongue, and gingival crevice, and the results were compared between older patients with RA and controls. SETTING: University of Michigan Medical Center, Ann Arbor, VA Medical Center, and University of Michigan School of Dentistry. PARTICIPANTS: A total of 111 community-dwelling subjects with a diagnosis of RA and 83 gender-matched control subjects. MEASUREMENTS: Colistin nalidixic acid agar plates with 5% sheep's blood were inoculated and incubated. Isolates were speciated using the API Staph Trac micro method and catalase and coagulase tests. MAIN RESULTS: Individuals with RA had a higher prevalence of S. aureus isolated from the oral cavity. However, only the oropharynx and tongue revealed higher rates; all other sites were insignificant. The presence of oral S. aureus was associated with xerostomia. Staphylococcus epidermidis was not detected from any of the oral sites sampled. Sixty-two percent (10/16) of the S. aureus isolates from the RA subjects were resistant to penicillin and ampicillin, whereas none were resistant to a cephalosporin. CONCLUSIONS: These findings suggest that rheumatoid arthritis may be a risk factor for LPJI in older prosthetic joint patients undergoing invasive dental procedure in the posterior oral cavity. This increased risk is caused, in part, by a higher prevalence of S. aureus in the posterior oral cavity. The prevalence and the antibiotic resistance of S. aureus must be considered when determining the need for chemoprophylaxis.

Group G streptococcal arthritis: case report and review of the literature.

Nongonococcal septic arthritis in adults is usually caused by infections with staphylococcal or streptococcal species. In patients with underlying diseases, especially those with chronic joint disease or malignancy, bacterial isolates from infected joint spaces may include group G streptococci. Occasionally, group G streptococcal arthritis may occur in otherwise healthy individuals. We report a case of pyogenic sacroiliitis in a healthy young adult and review the pertinent literature concerning group G streptococcal arthritis.

Colonization and transmission of high-level gentamicin-resistant enterococci in a long-term care facility.

OBJECTIVES: To assess the prevalence of high-level gentamicin-resistant enterococcus (HGRE) colonization, transmission patterns, and spectrum of illness among residents of a long-term care facility. DESIGN: Monthly surveillance for HGRE colonization of wounds, rectum, and perineum over a 1-year period. SETTING: A Veterans Affairs long-term care facility attached to an acute-care facility. PATIENTS: All 341 patients in the facility during the observation period. RESULTS: Over the 1-year period, 120 patients (35.2%) were colonized with HGRE at least once, with an overall monthly colonization rate of 20 +/- 1.5%. HGRE were isolated from rectum (12.8%), wounds (11.7%), and perineum (9.3%). Patients with the poorest functional status had the highest rate of colonization (P < 0.0005). HGRE-colonized patients were more likely to be colonized with methicillin-resistant Staphylococcus aureus (51% versus 25%; P < 0.0005). Seventy-four patients (21.7%) were colonized at admission or at the start of the study. Another 46 patients (13.5%) acquired HGRE during the study, including 36 who acquired HGRE while in the long-term care facility and 10 who were positive when transferred back from the acute-care hospital. Based on plasmid profiles, only two patients appeared to have isolates similar to those of current or previous roommates. Carriage of HGRE was transient in most cases. Only 20 patients were colonized for 4 or more months, and those patients usually carried different strains intermittently. Infections were infrequent, occurring in only 4.1% of total patients. CONCLUSIONS: In our long-term care facility, HGRE were endemic, and new acquisition of HGRE occurred frequently. However, only two patients had evidence of acquisition from a roommate, suggesting that cross-infection from a roommate was not a major route of spread of HGRE.