is an important pathogen responsible for 6% of infections in LTCFs.28
Here, we describe several cases of infection and/or colonization due to genetically related KPC-Kp strains occurring in a single LTACH. Our study emphasizes the following four important points.
First, the clinical isolates collected at the LTACH are genetically related to ST258, the dominant strain of KPC-Kp seen throughout the USA.4,6
This supports the earlier hypothesis by Endimiani et al.
that the acquisition of a blaKPC
gene, in addition to other potential resistant determinants, may confer on this isolate of K. pneumoniae
a marked selective advantage that is leading to its successful dissemination.
Secondly, we noted that the seven KPC-Kp strains found in the LTACH and FL-7 showed high-level resistance to carbapenems, whereas the remaining two KPC-Kp strains (FL-10 and FL-11) had imipenem MICs in the susceptible range by agar dilution.15
We show that the higher MIC levels observed in the first group are a result of the combination of an increased level of KPC expression and loss of the three OmpK proteins. Possessing at least one porin (e.g. OmpK-35) and having low-level KPC expression does not raise the carbapenem MICs within the resistant range. The loss of porins is very common in K. pneumoniae
However, this phenomenon combined with the presence of a KPC β-lactamase has been observed infrequently.2,18
Thirdly, the AST results support the notion that the therapeutic options against serious infections due to KPC-Kp strains are limited to tigecycline and colistin.4
However, tigecycline may not reach desired serum levels to treat systemic infections, leaving colistin as the ‘last choice’.31,32
Unfortunately, colistin-resistant KPC-Kp isolates have also been reported.33
Therefore, novel antibiotics or combinations with potent activity against infections due to KPC-Kp isolates need to be considered.34,35
Finally, we conclude this analysis by noting that the spread of KPC-Kp strains outside of the hospital setting (e.g. LTCFs, including LTACHs) is particularly alarming. As illustrated in this report, these patients moved frequently among hospitals, LTCFs and the community. This, like other studies, shows these patients to be elderly, with serious co-morbidities, and frequently requiring intravascular and bladder catheters.11,36
The occurrence of multidrug-resistant organisms (MDROs) in this population has been reported previously,37
mostly resulting from the transfer of patients colonized in the hospital setting to LTCFs and potentially to the community. The experiences with community-associated methicillin-resistant Staphylococcus aureus
and CTX-M-producing E. coli
isolates serve as harsh reminders that the community could potentially represent a critical reservoir for MDROs.38,39
On the other hand, the frail nature of patients in LTACHs, the excessive use of antibiotics and the difficulty in diagnosing infection versus colonization fosters an environment where isolates containing resistance mechanisms are selected and transmitted to other components of the healthcare system (the primary reservoir of resistance).11
Understanding the transmission dynamics of KPC-Kp among these different settings has therefore become critical.
We realize that the presence of KPC-Kp isolates in LTACHs poses a series of new and frightening challenges. The clinical outcome associated with KPC-Kp infections in hospitalized patients is poor.1,40–42
Although the high mortality reported here suggests this may be the case in other settings, the clinical impact of KPC-Kp on infected or colonized patients remains to be determined. Furthermore, the isolation of KPC-Kp strains results in therapeutic and infection control responses that require considerable effort, expertise and resources often not available outside of hospitals. For instance, colistin has emerged as the last option for infections caused by KPC-Kp.3
However, this antibiotic is perceived as a potentially nephrotoxic medication and patients usually need to be closely monitored while they receive this cationic polypeptide.32
Moreover, it is a common practice in hospitals to isolate patients harbouring KPC-Kp, a measure that may be difficult to implement in LTCFs.
A special challenge illustrated here is the control of the inter-institutional transfer of KPC-Kp. In this report we demonstrate that one patient (i.e. the patient harbouring isolate FL-7) was previously admitted to a hospital in Cleveland, OH, an endemic area of KPC-Kp transmission, and was subsequently transferred to one of the hospitals associated with the South Florida outbreak. Similar occurrences have been reported elsewhere.9,43
Furthermore, all patients tested at the LTACH were colonized in their gastrointestinal and/or urinary tract. However, we do not have a clear explanation why active surveillance did not detect any colonized patient apart from those detected by clinical samples. It should be noted that colonization might promote the spread of KPC-Kp isolates in the community.1
In one recent report, a patient residing in the community probably acquired the KPC-Kp from his wife, who was a documented carrier of this organism as a result of her hospitalization in a tertiary-care hospital in Israel.44
As demonstrated previously, performing surveillance in patients admitted from geographic areas with high-level rates of KPC-Kp infection/colonization (e.g. eastern USA) or before discharging them into the community might be a necessary infection control practice.27,45
In this case, implementation of CDC guidelines (i.e. active surveillance with rectal swabs along with enhanced infection-control practices) helped end the KPC-Kp outbreak at the LTACH in early April 2008.27
Whether attempts should be made to decolonize patients with such MDROs still remains an open question, and procedures and guidelines may need to be established. The speed and fury by which the epidemic of KPC-Kp is spreading in North America mandates urgent action.