To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
To assess whether measurement and feedback of chlorhexidine gluconate (CHG) skin concentrations can improve CHG bathing practice across multiple intensive care units (ICUs).
A before-and-after quality improvement study measuring patient CHG skin concentrations during 6 point-prevalence surveys (3 surveys each during baseline and intervention periods).
The study was conducted across 7 geographically diverse ICUs with routine CHG bathing.
Adult patients in the medical ICU.
CHG skin concentrations were measured at the neck, axilla, and inguinal region using a semiquantitative colorimetric assay. Aggregate unit-level CHG skin concentration measurements from the baseline period and each intervention period survey were reported back to ICU leadership, which then used routine education and quality improvement activities to improve CHG bathing practice. We used multilevel linear models to assess the impact of intervention on CHG skin concentrations.
We enrolled 681 (93%) of 736 eligible patients; 92% received a CHG bath prior to survey. At baseline, CHG skin concentrations were lowest on the neck, compared to axillary or inguinal regions (P < .001). CHG was not detected on 33% of necks, 19% of axillae, and 18% of inguinal regions (P < .001 for differences in body sites). During the intervention period, ICUs that used CHG-impregnated cloths had a 3-fold increase in patient CHG skin concentrations as compared to baseline (P < .001).
Routine CHG bathing performance in the ICU varied across multiple hospitals. Measurement and feedback of CHG skin concentrations can be an important tool to improve CHG bathing practice.
A cross-sectional survey study of inpatient prescribers in a university health system was performed to assess the importance they place on different clinical risk factors when making empiric antibiotic decisions. Our findings show that these clinical risk factors were weighted differently based on the clinical scenario and the type of prescriber.
An improved understanding of carbapenem-resistant Klebsiella pneumoniae (CRKP) in long-term acute care hospitals (LTACHs) is needed. The objective of this study was to assess risk factors for colonization or infection with CRKP in LTACH residents.
A case-control study was performed at a university-affiliated LTACH from 2008 to 2013. Cases were defined as all patients with clinical cultures positive for CRKP and controls were those with clinical cultures positive for carbapenem-susceptible K. pneumoniae (CSKP). A multivariate model was developed to identify risk factors for CRKP infection or colonization.
A total of 222 patients were identified with K. pneumoniae clinical cultures during the study period; 99 (45%) were case patients and 123 (55%) were control patients. Our multivariate analysis identified factors associated with a significant risk for CRKP colonization or infection: solid organ or stem cell transplantation (OR, 5.05; 95% CI, 1.23–20.8; P=.03), mechanical ventilation (OR, 2.56; 95% CI, 1.24–5.28; P=.01), fecal incontinence (OR, 5.78; 95% CI, 1.52–22.0; P=.01), and exposure in the prior 30 days to meropenem (OR, 3.55; 95% CI, 1.04–12.1; P=.04), vancomycin (OR, 2.94; 95% CI, 1.18–7.32; P=.02), and metronidazole (OR, 4.22; 95% CI, 1.28–14.0; P=.02).
Rates of colonization and infection with CRKP were high in the LTACH setting, with nearly half of K. pneumoniae cultures demonstrating carbapenem resistance. Further studies are needed on interventions to limit the emergence of CRKP in LTACHs, including targeted surveillance screening of high-risk patients and effective antibiotic stewardship measures.
Pasteurella multocida (“killer of many species”) is a nonmotile, gram-negative, facultative coccobacillus best known for its association with soft-tissue infections after animal bites. However, this organism is also capable of causing invasive and life-threatening infections.
Pasteurella multocida is found worldwide. It commonly colonizes the upper respiratory tract of many animals, most notably cats (70% to 90%) and dogs (50% to 66%). Human infection is usually related to animal exposure. The most common mode of transmission to humans is by direct inoculation by a bite or scratch. Inoculation can also occur by nontraumatic animal contact, such as when a wound is licked by an animal. The second mode of transmission is by colonization of the human respiratory tract occurring with exposure to animals such as nuzzling or grooming of pets. Pasteurella has been cultured from the respiratory tract of healthy veterinary workers and animal handlers as well as from ill patients. Infections can occasionally occur in the absence of animal contact.
There are several species and subspecies of Pasteurella, with the most common ones causing human disease being P. multocida subsp. multocida, P. multocida subsp. septica, Pasteurella dagmatis, Pasteurella canis, and Pasteurella stomatis. These organisms can resemble Haemophilus and Neisseria species when visualized on Gram stain, grow well on sheep and chocolate agar, and appear as smooth, mucoid blue colonies.
Most of the virulence factors have been studied in animals. Pathogenesis of Pasteurella depends on the bacteria’s ability to adhere to the host’s respiratory epithelium, typically the tonsils, which can be mediated through fimbrae. Some species are capable of producing a leukotoxin that affects leukocytes and inhibits cellular immune responses. Differences between virulent strains of Pasteurella are identified according to capsular antigens A to F, which cause different animal diseases.
Pasteurella multocida (“killer of many species”) is a gram-negative, pleomorphic coccobacillus best known for its association with soft-tissue infections after animal bites. However, this organism is also capable of causing invasive and life-threatening infections.
Pasteurella multocida is found worldwide. It commonly colonizes the upper respiratory tract of many animals, most notably cats (70% to 90%) and dogs (50% to 66%). Human infection is usually related to animal exposure. Direct inoculation by a bite or scratch is the most common mode of transmission of P. multocida to humans. Inoculation can also occur by nontraumatic animal contact, such as when a wound is licked by an animal. The second mode of transmission is by colonization of the human respiratory tract occurring with exposure to animals such as nuzzling or grooming of pets. The organism has been cultured from the respiratory tract of healthy veterinary workers and animal handlers as well as from ill patients. Infections can also occasionally occur with no history of animal contact.
There are several species and subspecies of Pasteurella, but the most common ones causing human disease are P. multocida, Pasteurella dagmatis, Pasteurella canis, and Pasteurella stomatis. These organisms are nonmotile, gram-negative facultative anaerobes that on Gram stain can resemble Haemophilus and Neisseria species. The organism grows well on sheep and chocolate agar and appears as watery mucoid blue colonies.
Email your librarian or administrator to recommend adding this to your organisation's collection.