Carbapenem-resistant enterobacteriaceae
[7] When compared to other hospitalized patients, those admitted from long-term acute care (LTAC) facilities have significantly higher incidence of colonization and infection rates.
[7] Infections with carbapenem-resistant Klebsiella pneumoniae were associated with organ/stem cell transplantation, mechanical ventilation, exposure to antimicrobials, and overall longer length of stay in hospitals.
[10] In a study carried out at Sheba medical center, there was a trend toward worse Charleson Comorbidity scores in patients who acquired CRKP during ICU stay.
[11] Those at highest risk are patients receiving an organ or stem cell implantation, use of mechanical ventilation, or have to have an extended stay in the hospital along with exposure to antimicrobials.
Policies regarding contact precaution for patients infected or colonized by gram-negative pathogens were also observed in hospitals reporting decreases in CRE prevalence.
In one study, an elderly patient with acute lymphoblastic leukemia being treated in a long-term care facility contracted a CRE infection.
One study from Japan found that 6.4% of healthy adults carried ESBL (mostly cefotaximase)-producing strains compared to 58.4% in Thailand, where antibiotics are available over the counter and without prescription.
[16] The FDA's safety communication came a day after the UCLA Health System, Los Angeles, notified more than 100 patients that they may have been infected with CRE during endoscopies between October 2014 and January 2015.
[citation needed] The β-lactam family of antibiotic molecules consists of four groups: penicillins, cephalosporins, carbapenems (such as imipenem, ertapenem, meropenem and doripenem) and monobactams.
They enter the periplasmic space through porins, where they then inhibit transpeptidases (which are also known as penicillin-binding proteins (PBPs)), enzymes that facilitate peptide cross-links during cell wall synthesis.
[citation needed] A unique quality of carbapenems is their resistance to hydrolysis by bacterial plasmid and chromosomally mediated extended-spectrum β-lactamases (ESBL).
[33] At the UVA Medical Center, a transfer mechanism of KPC-dependent carbapenem resistance was discovered in the transmission of a plasmid carrying the transposon (Tn4401), which contains the KPC gene (blaKPC), to several bacteria including Enterobacter cloacae, Klebsiella oxytoca, E. coli, and Citrobacter freundii.
The blaOXA genes which encode OXA β-lactamases are found on both chromosomes and plasmids, and they have their natural reservoir in environmental bacteria and deep-sea microflora.
[33] The facilitated spread of carbapenem resistance appears to have multiple origins and repeated introduction into the UK of bacteria with the blaOXA-48 gene via horizontal transfer of similar plasmids to pOXA-48a.
A recent study in the UK examined 26 isolates of Enterobacteriaceae consisting of a diverse set of sequence types (ST) of K. pneumoniae, E. coli, and Enterobacter cloacae producing OXA-48-like carbapenemases.
Following incubation, the zones of inhibition surrounding the various antibiotic discs are measured and compared with Clinical and Laboratory Standard Institute guidelines.
[34] Another study used matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) to determine resistance patterns in bacteria from freshly positive blood cultures.
[citation needed] MALDI-TOF cannot detect resistant bacteria, which do not physically disrupt the β-lactam antibiotic, i.e. where no mass change occurs.
Due to the bacterial resistance to cleaning measures, staff should take extreme precaution in maintaining sterile environments in hospitals not yet infected with the CRE-resistant bacteria.
[43] Although a consensus exists for the need of prevention protocols, infection control practices often vary among hospitals, even within close geographic area.
[45] Many public health initiatives are moving towards a more standardized approach at multiple levels: among local facilities (especially long-term and acute care), regional hospitals, national institutions, and global practices.
The comprehensive plan included guidelines for cohorting patients in separate locations, cleaning with 1,000 ppm hypochlorite, screening for isolates from rectal swabs, and distribution of educational instruction sheets, lectures for all medical staff, and training.
Specific methods included implementing an objective evaluation process, environmental surfaces staff education, programmatic feedback, and continuous training to minimize the spread of hospital-associated infections.
Fosfomycin is an antimicrobial agent that acts to inhibit UDP-N-acetylglucosamine enolpyruvyl transferase (MurA) which catalyzes one of the early steps of bacterial cell wall synthesis, and is effective against gram-negative and -positive aerobic bacteria, such as CRE.
[citation needed] The elevated level of antimicrobial activity by fosfomycin can be attributed to the fact that resistance to this antibiotic in Enterobacteriaceae is chromosomally encoded and not plasmid-mediated.
Both urinary tract and primary blood infections can make tigecycline ineffective, because it has limited penetration and rapid tissue diffusion after being intravenously infused, respectively.
[48] In a separate study, CRE were treated with colistin, amikacin, and tigecycline, and emphasizes the importance of using gentamicin in patients undergoing chemotherapy or stem-cell therapy procedures.
[10] According to the U.S. Centers for Disease Control, CRE producing what was the most common type of carbapenem-destroying enzyme in 2001 were first detected in a North Carolina hospital in 1996.
[40] Hospital handwashing stations were found to be environmental reservoirs for CRE after screening all wet-area locations, including sinks, water fountains, and ice machines.
This can be very important in future clinical and community settings, as an increase in copper utilization in hospital room equipment could help to greatly reduce the spread of antibiotic-resistant infection and the horizontal gene transfer of this antibiotic resistance.
