Yuan-Chih Mao1, Chin-Lu Chang2, Yhu-Chering Huang3, Lin-Hui Su4, Chao-Tai Lee5. 1. Department of Hepatogastroenterology, Tainan Municipal Hospital, Tainan, Taiwan; Department of Internal Medicine, Tainan Municipal Hospital, Tainan, Taiwan. 2. Department of Internal Medicine, Tainan Municipal Hospital, Tainan, Taiwan; Department of Infectious Diseases, Tainan Municipal Hospital, Tainan, Taiwan. 3. Division of Pediatric Infectious Diseases, Department of Pediatrics, Chang Gung Memorial Hospital at Linkou, Kweishan, Taoyuan, Taiwan; Chang Gung University College of Medicine, Kweishan, Taoyuan, Taiwan. 4. Chang Gung University College of Medicine, Kweishan, Taoyuan, Taiwan; Department of Laboratory Medicine, Chang Gung Memorial Hospital at Linkou, Kweishan, Taoyuan, Taiwan. Electronic address: sulinhui@gmail.com. 5. Department of Clinical Laboratory, Tainan Municipal Hospital, Tainan, Taiwan. Electronic address: chaotai2010@yahoo.com.tw.
Abstract
BACKGROUND: Providencia stuartii survives well in natural environment and often causes opportunistic infection in residents of long-term care facilities (LTCFs). Clinical isolates of P. stuartii are usually resistant to multiple antibiotics. The bacterium is also naturally resistant to colistin and tigecycline. Treatment of infections caused by carbapenem-resistant P. stuartii is challenging. METHODS: During a 15-month period in 2013-2014, four isolates (P1, P2, and P3B/P3U) of P. stuartii showing intermediate resistance to imipenem were identified at a regional hospital in southern Taiwan. They were identified from three patients (P1-P3) transferred from the same LTCF for the treatment of the infection. Pulsed-field gel electrophoresis was used to genotype the isolates. Resistance genes/plasmids and outer membrane proteins were investigated by polymerase chain reaction and sequence analysis. RESULTS: Isolates P1 and P3B/P3U demonstrated similar pulsotypes. All isolates were found to have resistance genes (blaCMY-2, qnrD1, aac(6')-Ib-cr) carried on nonconjugative IncA/C plasmids of different sizes. A single point mutation was identified in the chromosomal gyrA (Ser83Ile) and parC (Ser84Ile) genes of all isolates. Various point mutations and insertion/deletion changes were found in their major outer membrane protein gene ompPst1. CONCLUSIONS: Isolates of similar pulsotypes could appear after 15 months and caused urosepsis in another resident of the same LTCF. The bacterium may have persisted in the environment and caused opportunistic infection. As LTCF residents are usually vulnerable to infections, surveillance of multidrug-resistant organisms and infection control intervention that have been established in acute-care hospitals to control infections by resistant organisms are apparently as essential in LTCFs.
BACKGROUND:Providencia stuartii survives well in natural environment and often causes opportunistic infection in residents of long-term care facilities (LTCFs). Clinical isolates of P. stuartii are usually resistant to multiple antibiotics. The bacterium is also naturally resistant to colistin and tigecycline. Treatment of infections caused by carbapenem-resistant P. stuartii is challenging. METHODS: During a 15-month period in 2013-2014, four isolates (P1, P2, and P3B/P3U) of P. stuartii showing intermediate resistance to imipenem were identified at a regional hospital in southern Taiwan. They were identified from three patients (P1-P3) transferred from the same LTCF for the treatment of the infection. Pulsed-field gel electrophoresis was used to genotype the isolates. Resistance genes/plasmids and outer membrane proteins were investigated by polymerase chain reaction and sequence analysis. RESULTS: Isolates P1 and P3B/P3U demonstrated similar pulsotypes. All isolates were found to have resistance genes (blaCMY-2, qnrD1, aac(6')-Ib-cr) carried on nonconjugative IncA/C plasmids of different sizes. A single point mutation was identified in the chromosomal gyrA (Ser83Ile) and parC (Ser84Ile) genes of all isolates. Various point mutations and insertion/deletion changes were found in their major outer membrane protein gene ompPst1. CONCLUSIONS: Isolates of similar pulsotypes could appear after 15 months and caused urosepsis in another resident of the same LTCF. The bacterium may have persisted in the environment and caused opportunistic infection. As LTCF residents are usually vulnerable to infections, surveillance of multidrug-resistant organisms and infection control intervention that have been established in acute-care hospitals to control infections by resistant organisms are apparently as essential in LTCFs.