Colonization of skilled-care facility residents with antimicrobial-resistant pathogens.

OBJECTIVES: To determine the frequency of and risk factors for colonization of skilled-care unit residents by several antimicrobial-resistant bacterial species, methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococcus (VRE), or extended-spectrum-beta-lactamase-producing (ESBL-producing) (ceftazidime resistant) Klebsiella pneumoniae or Escherichia coli. DESIGN: Point-prevalence survey and medical record review. SETTING: The skilled-care units in one healthcare facility. PARTICIPANTS: 120 skilled-care unit residents. MEASUREMENTS: Colonization by each of the four antimicrobial-resistant pathogens during a point-prevalence survey, using rectal, nasal, gastrostomy-tube site, wound, and axillary cultures, June 1-3, 1998; 117 (98%) had at least one swab collected and 114 (95%) had a rectal swab collected. Demographic and clinical characteristics were evaluated as risk factors for colonization. All isolates were strain typed by pulsed-field gel electrophoresis of total genomic deoxyribonucleic acid. RESULTS: Of 117 participants, 50 (43%) were culture positive for > or =1 antimicrobial-resistant pathogen: MRSA (24%), ESBL-producing K. pneumoniae (18%) or E. coli (15%), and VRE (3.5%). Of 50 residents culture positive for any of these four antimicrobial-resistant species, 13 (26%) were colonized by more than one resistant species; only three (6%) were on contact-isolation precautions at the time of the prevalence survey. Risk factors for colonization varied by pathogen: total dependence on healthcare workers (HCWs) for activities of daily living (ADLs) and antimicrobial receipt for MRSA, total dependence on HCWs for ADLs for ESBL-producing K. pneumoniae, and antimicrobial receipt for VRE. No significant risk factors were identified for colonization by ESBL-producing E. coli. Among colonized patients, there was a limited number of strain types for MRSA (24 patients, 4 strain types) and ESBL-producing K. pneumoniae (21 patients, 3 strain types), and a high proportion of unique strain types for VRE (4 patients, 4 strain types) and FSBL-producing E. coli (17 patients, 10 strain types). CONCLUSION: A large unrecognized reservoir of skilled-care-unit residents was colonized by antimicrobial-resistant pathogens, and co-colonization by more than one target species was common. To prevent transmission of antimicrobial-resistant pathogens in long-term care facilities in which residents have high rates of colonization, infection-control strategies may need to be modified. Potential modifications include enhanced infection-control strategies, such as universal gloving for all or high-risk residents, or screening of high-risk residents, such as those with total dependence on HCWs for ADLs or recent antimicrobial receipt, and initiation of contact-isolation precautions for colonized residents.

Rhodococcus meningitis in an immunocompetent host.

Rhodococcus species are increasingly being recognized as pathogens, especially in patients infected with the human immunodeficiency virus. Most cases of rhodococcus infection in these patients are due to Rhodococcus equi and involve the lungs. CNS infections due to Rhodococcus species are rare, and meningitis due to non-equi Rhodococcus has never been reported in a healthy host. We report a case of meningitis due to non-equi Rhodococcus in a previously healthy 24-year-old woman. We also review and summarize the reported cases of CNS infections caused by Rhodococcus species.

Nosocomial infections in human immunodeficiency virus-infected patients in a long-term-care setting.

To our knowledge, the epidemiology of hospital-acquired infections in human immunodeficiency virus (HIV)-infected patients during long-term care has not been reported. For 13 months, we observed HIV-infected patients (50 men and 15 women) in a dedicated 21-bed unit in a long-term-care facility to determine the rate of nosocomial infections. The mean age of the patients was 39 years (range, 22-78 years); 74% of the patients had CD4 cell counts of < 200/mm3. There was a total of 152 infections (24 infections per 1,000 long-term-care days). The factors associated with the occurrence of a nosocomial infection were low CD4 cell counts, poor functional status, and longer duration of stays at the facility. The three most common infections were Clostridium difficile-associated diarrhea, primary bacteremia, and urinary tract infection. Eighteen hospital-manifested opportunistic infections occurred. More than 50% of the cases of bacteremia were due to multidrug-resistant organisms. Nosocomial infections occur commonly in HIV-infected patients in long-term care and thus are important considerations in patient management.

Hyperferritinemia in reactive hemophagocytic syndrome report of four adult cases.

Four patients were diagnosed with reactive hemophagocytic syndrome (RHPS) during a 7 month period. Of these, three patients were diagnosed with acquired immunodeficiency syndrome complicated by disseminated Mycobacterium tuberculosis infection, incompletely treated Pneumocystis carinii pneumonia and disseminated histoplasmosis respectively. The fourth patient had non-Hodgkin's lymphoma of the mature T-cell phenotype. Fever, bicytopenia, or pancytopenia, elevated serum lactate dehydrogenase (LDH) level (> 1,000 IU/L), and hemophagocytic histiocytosis in smears of bone marrow aspirate were present in all patients. Hyperferritinemia (> 10,000 ng/ml) was present in all (range 34,976 to 425,984 ng/mL) and showed a decrease in the two patients who responded to therapy. Hyperferritinemia (> 10,000 ng/ml) and elevated serum LDH (> 1,000 IU/L) are important clues to the diagnosis of RHPS in the febrile cytopenic patient with immunodeficiency.

Infective endocarditis in injection drug users: importance of human immunodeficiency virus serostatus and degree of immunosuppression.

Human immunodeficiency virus (HIV)-infected patients are at increased risk for serious and recurrent bacterial infections. We hypothesized that the degree of immunosuppression may play an important role in outcomes for HIV-seropositive patients with infective endocarditis (IE). To test our hypothesis, we retrospectively reviewed 144 cases of IE in injection drug users. One hundred two patients with documented HIV status (45 HIV-seropositive patients and 57 HIV-seronegative patients) were included in the analysis. Eleven patients (6 HIV-seropositive patients and 5 HIV-seronegative patients) died in the hospital. Staphylococcus aureus, the most common etiologic pathogen causing IE in our series, was isolated from 32 HIV-seropositive patients (71.1%) and 32 HIV-seronegative patients (56.1%). A clear inverse correlation between mortality rate and CD4 cell count was demonstrated (r = -.625; P < .001). Both univariate and multivariate analyses supported the finding of significantly higher mortality rates among patients with CD4 cell counts of < 200/mm3 than among patients with CD4 cell counts of > 500/mm3 (OR, 14.7; 95% CI, 2.64-81.9).

Specimen contamination in mycobacteriology laboratory detected by pseudo-outbreak of multidrug-resistant tuberculosis: analysis by routine epidemiology and confirmation by molecular technique.

A cluster of multidrug-resistant tuberculosis sputum isolates led to the detection of specimen contamination in a hospital mycobacteriology laboratory. Thirteen specimens were smear negative but culture positive from one specimen only; 12 appeared to be contaminated. Each of these specimens was processed in the same batch as one or more smear- and culture-positive isolates. Molecular analysis confirmed the traditional epidemiologic, laboratory, and clinical methods of evaluating presumed mycobacterial contamination.

Depressed neutrophil superoxide production in human immunodeficiency virus infection.

Neutrophil (PMNL) superoxide (O2-) production was evaluated in 71 patients with human immunodeficiency virus (HIV) infection at different stages of disease. In vitro O2- production was significantly depressed for PMNL isolated from HIV-positive patients compared with control PMNL at rest and after stimulation. The degree of impairment of O2- production was more pronounced for patients with lower absolute CD4+ lymphocyte counts. Antiretroviral therapy with zidovudine was also associated with impaired O2- production, but this may reflect a longer duration of disease for treated patients. Zidovudine had no direct inhibitory effect on O2- production by control PMNL in vitro, and serial measurements of O2- production by PMNL from patients before and after initiation of zidovudine did not demonstrate an in vivo inhibitory effect. Impaired PMNL oxidative metabolism in HIV infection may contribute to the increased risk of serious bacterial infections, certain opportunistic infections, and perhaps the pathogenesis of HIV infection itself.

Reactive hemophagocytic syndrome: a new presentation of disseminated histoplasmosis in patients with AIDS.

We report the cases of six patients with AIDS in whom reactive hemophagocytic syndrome (RHPS) secondary to disseminated histoplasmosis was diagnosed. RHPS was diagnosed by established criteria, including fever (duration of > or = 7 days, with peak temperatures of > 38.5 degrees C), unexplained thrombocytopenia with anemia and/or neutropenia, and bone marrow biopsy findings of hemophagocytic histiocytosis. Disseminated Histoplasma capsulatum infection was diagnosed on the basis of the results of cultures of the bone marrow sample. The serum lactate dehydrogenase (LDH) level was elevated (> 1,000 IU/L) in all patients, and five of six patients had hyperferritinemia (range of ferritin level, 15,848-425,984 ng/mL). Five patients had features resembling severe sepsis with multiorgan dysfunction. Three patients recovered, and the findings of RHPS resolved following therapy with amphotericin B. In patients with AIDS, the combination of fever, cytopenia, elevated serum LDH level (> 1,000 IU/L), and/or hyperferritinemia (ferritin level of > 10,000 ng/mL) is a clue to the diagnosis of RHPS and disseminated histoplasmosis; bone marrow biopsy is valuable in establishing the diagnosis.