RESUMEN
BACKGROUND: Infection with fluoroquinolone-resistant strains of salmonella is rare, as is nosocomial salmonella infection. We describe the first recognized outbreak of fluoroquinolone-resistant salmonella infections in the United States, which occurred in two nursing homes and one hospital in Oregon. METHODS: We interviewed medical staff and reviewed patients' charts and death certificates. In Nursing Home A we conducted a case-control study. Patients were defined as residents of the nursing home from whom fluoroquinolone-resistant Salmonella enterica serotype Schwarzengrund was isolated between February 1996 and December 1998. Controls were residents with similar medical conditions whose cultures did not yield salmonella. We compared isolates using pulsed-field gel electrophoresis and sequence analysis. We reviewed pharmacy records to compare the use of fluoroquinolone among several nursing homes. RESULTS: Eleven patients with fluoroquinolone-resistant salmonellosis were identified at two nursing homes. The index patient had been hospitalized in the Philippines and had probably acquired the infection there. Transmission was probably direct (from patient to patient) or through contact with contaminated surfaces. Treatment with fluoroquinolones during the six months before a culture was obtained was associated with a significant risk of salmonella infection (4 of 5 patients had taken fluoroquinolones, as compared with 2 of 13 controls; odds ratio, 22.0; 95 percent confidence interval, 1.06 to 1177). The patients were not significantly more likely than the controls to have taken other antibiotics. More fluoroquinolones were used at Nursing Home A than at similar nursing homes in Oregon. The isolates from the outbreak had similar patterns on pulsed-field gel electrophoresis and the same gyrA mutations. The isolates from the outbreak were also similar to the only previous isolate of fluoroquinolone-resistant salmonella in the United States, which came from a patient in New York who had been transferred from a hospital in the Philippines. CONCLUSIONS: We describe a prolonged nosocomial outbreak of infection with fluoroquinolone-resistant S. enterica serotype Schwarzengrund. More such outbreaks are likely in institutional settings, particularly those in which there is heavy use of antimicrobial agents.
Asunto(s)
Antiinfecciosos/uso terapéutico , Infección Hospitalaria/epidemiología , Brotes de Enfermedades , Infecciones por Salmonella/epidemiología , Salmonella enterica , Anciano , Anciano de 80 o más Años , Antiinfecciosos/farmacología , Estudios de Casos y Controles , Infección Hospitalaria/microbiología , Infección Hospitalaria/transmisión , Transmisión de Enfermedad Infecciosa , Farmacorresistencia Microbiana , Utilización de Medicamentos/estadística & datos numéricos , Electroforesis en Gel de Campo Pulsado , Femenino , Fluoroquinolonas , Hospitales , Humanos , Masculino , Pruebas de Sensibilidad Microbiana , Persona de Mediana Edad , Casas de Salud , Oregon/epidemiología , Factores de Riesgo , Infecciones por Salmonella/microbiología , Infecciones por Salmonella/transmisión , Salmonella enterica/clasificación , Salmonella enterica/efectos de los fármacos , Salmonella enterica/aislamiento & purificaciónRESUMEN
CONTEXT: In December 1995, reported Salmonella enterica serotype Newport (SN) infections increased sharply in Oregon and British Columbia but not elsewhere in North America. Similar unexplained increases had been noted in 6 other states in the fall of 1995. OBJECTIVE: To determine the source of the outbreak(s). DESIGN: Case-control studies, environmental investigations, bacterial subtyping, and surveillance information review. SETTINGS: Oregon and British Columbia communities (winter 1995-1996) and Georgia, Oklahoma, Pennsylvania, Vermont, Virginia, and West Virginia (fall 1995). PARTICIPANTS: Oregon and British Columbia residents with culture-confirmed SN infections and onset from December 1, 1995, through February 29, 1996, and healthy community controls. MAIN OUTCOME MEASURES: Odds ratio (OR) of illness associated with exposures; distribution patterns and culture of alfalfa seeds and sprouts; subtyping of SN isolates. RESULTS: We identified 133 cases in Oregon and British Columbia; 124 (93%) occurred in patients older than 18 years; 87 (65%) were female. Case patients were more likely than community control subjects to report having eaten alfalfa sprouts in the 5 days preceding illness (41% [17/41] vs 4% [3/75]; OR, 17.0; 95% confidence interval, 4.3-96.0). Case isolates shared a distinctive pulsed-field gel electrophoresis (PFGE) pattern. The SN was grown from seeds and alfalfa sprouts. The distribution of 1 seed lot to multiple growers corresponded to the distribution of cases. Distribution of a second seed lot from the same European wholesaler corresponded to the location of the fall outbreak, which was characterized by a similar demographic profile. The PFGE pattern of fall outbreak isolates and confiscated sprouts and seeds was indistinguishable from the Oregon and British Columbia outbreak and differed from background isolates. CONCLUSIONS: The SN-contaminated alfalfa seeds were distributed to multiple growers across North America in 1995 and resulted in a protracted international outbreak scattered over many months. Current sprouting methods are inadequate to protect consumers from such events. Alfalfa sprouts may be an elusive but important vehicle for salmonellosis and other enteric infections.
Asunto(s)
Brotes de Enfermedades , Medicago sativa/microbiología , Intoxicación Alimentaria por Salmonella/epidemiología , Salmonella enterica/clasificación , Semillas/microbiología , Estudios de Casos y Controles , Electroforesis en Gel de Campo Pulsado , Femenino , Humanos , Masculino , Intoxicación Alimentaria por Salmonella/etiología , Serotipificación , Estados Unidos/epidemiologíaRESUMEN
OBJECTIVE: To investigate a 1995 outbreak of Escherichia coli O157:H7 infections and to assess the safety of meat dehydration methods. DESIGN: Survey subsequent to routine surveillance report, environmental investigations, and laboratory experimentation. SETTING: Oregon community. PARTICIPANTS: Members of an extended household and their social contacts with confirmed or presumptive E coli O157:H7 infections. RESULTS: A total of 6 confirmed and 5 presumptive cases were identified. Homemade venison jerky was implicated as the source of transmission. E coli O157:H7 with the same distinctive, pulsed-field gel electrophoresis pattern seen in the case isolates was recovered from leftover jerky, uncooked meat from the same deer, a saw used to dismember the carcass, and fragments of the deer hide. In a subsequent survey, E coli O157:H7 was recovered from 3 (9%) of 32 deer fecal pellets collected in nearby forest land. In the laboratory, inoculated venison was dried at several time and temperature combinations, ranging up to 10 hours at 62.8 degrees C. Viable organisms were recovered under all conditions tested. CONCLUSIONS: Deer can be colonized by E coli O157:H7 and can be a source of human infections. Conditions necessary to ensure the safety of dried meat deserve further review. Game should be handled with the same caution indicated for commercially slaughtered meat.
Asunto(s)
Ciervos , Infecciones por Escherichia coli/epidemiología , Escherichia coli O157/aislamiento & purificación , Enfermedades Transmitidas por los Alimentos/epidemiología , Carne/microbiología , Adolescente , Adulto , Animales , Técnicas de Tipificación Bacteriana , Niño , Preescolar , Ciervos/microbiología , Diarrea/microbiología , Brotes de Enfermedades , Infecciones por Escherichia coli/etiología , Manipulación de Alimentos , Enfermedades Transmitidas por los Alimentos/etiología , Humanos , Lactante , Persona de Mediana Edad , Oregon/epidemiologíaRESUMEN
We have reviewed the structure, function, and biogenesis of mammalian cytochrome c oxidase, examined the tissue-specific expression of isoforms of cytochrome c oxidase subunits in different mammals, and attempted to correlate the data with our knowledge of cytochrome c oxidase deficiency, illustrated by one particular patient. Cytochrome c oxidase was isolated from bovine tissues, and individual subunits examined by SDS-PAGE, N-terminal peptide sequencing, and antibody binding. Isoforms of subunits VIa, VIIa, and VIII were identified, manifesting one pattern of expression in heart and skeletal muscle, and another in liver, kidney, and brain. In rat heart and liver, only one form of subunit VIIa was identified. Northern analysis of bovine and rat tissues suggested that the tissue-specific expression of subunits VIa and VIII is regulated transcriptionally in liver, kidney, and brain, and posttranscriptionally in heart and skeletal muscle. In humans, antibody binding documented isoforms of subunits VIa and VIIa, with the pattern of expression in heart and skeletal muscle differing from that in liver, kidney, and brain; our data suggested that both isoforms of subunit VIa may be expressed in human heart. In a patient with cytochrome c oxidase deficiency, the clinical, morphologic, and biochemical manifestations were much more severe in heart than in skeletal muscle. Antibody binding suggested partial assembly of the enzyme in heart. These and other data suggest considerably more variability in the tissue-specific expression of isoforms of cytochrome c oxidase subunits than previously recognized.