Outbreak of an armA Methyltransferase-Producing ST39 Klebsiella pneumoniae Clone in a Pediatric Algerian Hospital

Abstract

Here we report an outbreak of Klebsiella pneumoniae infections harboring extended spectrum β-lactamases (ESBL) and armA 16Sr RNA methylase that were detected in pediatric and neonatal intensive care units during the 2010 and 2011 surveys of 100 clinical strains of K. pneumoniae from Annaba hospitals in Algeria. Antibiotic susceptibility testing was performed using the disk diffusion method. Minimum inhibitory concentrations of three classes of antibiotics were determined using the E. test. Standard polymerase chain reaction amplification and sequencing were performed using primers targeting ESBL, 16S ribosomal RNA (rRNA) methyltransferases, aminoglycoside-modifying enzymes (AMEs), and quinolone encoding genes. Clonal relationships among the clinical isolates were performed using multilocus sequence typing. From our clinical isolates, we found high rates of antimicrobial resistance that were linked to the presence of different ESBL encoding genes and AMEs, including 23 strains that harbored several ESBL encoding genes along with the 16S rRNA methyltransferase armA. Among these isolates, we identified a cluster of eight isolates of the ST39 clone between February and June 2010 in a pediatric ward, suggesting that an outbreak had occurred during this period. In conclusion, the emergence of multidrug-resistant clones, which were likely responsible for a nosocomial outbreak, is worrying because there are already limited options in those critical situations. Finally, we believe that surveillance should be implemented to monitor the risk of emergence and spread of carbapenemases in Algeria.

Clonal Spread of 16S rRNA Methyltransferase-Producing Klebsiella pneumoniae ST37 with High Prevalence of ESBLs from Companion Animals in China

“…Reports on the prevalence of the 16S-RMTases have increased in the past years with the majority focused on the human clinical isolates including K. pneumoniae (Mezzatesta et al, 2013; Belbel et al, 2014; Bartoloni et al, 2016). Moreover, the majority of reports on dissemination of armA and rmtB to various Enterobacteriaceae species were focused on E. coli isolated from chickens and pigs (Yao et al, 2011; Yang Y. et al, 2015).…”

MALDI-TOF MS as a Tool To Detect a Nosocomial Outbreak of Extended-Spectrum-β-Lactamase- and ArmA Methyltransferase-Producing Enterobacter cloacae Clinical Isolates in Algeria

“…The presence of aadA1, aadA2, and ant2 in E. cloacae is exclusively described in this study. aadA2 and aadA1 were recently described in K. pneumoniae (12) in Algeria, and another variant (aadA6) was detected in Pseudomonas aeruginosa strains in Korea (25). MALDI-TOF MS has been successfully used for the identification of E. cloacae (26).…”

“…Indeed, this clade suggests the occurrence of an outbreak in this uro-nephrology unit within a period of 4 months, between November 2012 and February 2013, with an unknown common source of transmission. The transmission could be due to hand carriage by paramedical personnel (12,21) or a contaminated cytoscope, which is typically used to place double J catheters, especially in urology clinics (21).…”

“…This situation can promote the rapid dissemination of armA in various members of the Enterobacteriaceae family (23) (K. pneumoniae in Algeria [12], Escherichia coli, A. baumannii, and Serratia in China [30]). …”

“…Some recent investigations reported in Algeria have revealed an increase in ESBLproducing E. cloacae, with bla CTX-M1 , bla CTX-M3 , bla CTX-M15 , bla VEB-1 , bla , and bla TEM (9,10) being the most frequent genes detected. However, the epidemiology and molecular support of resistance to aminoglycosides due to AMEs in E. cloacae have never been studied in Algeria, even though they have been reported recently in Acinetobacter baumannii and Klebsiella pneumoniae (11,12). Indeed, we recently reported an outbreak in a pediatric Algerian hospital of K. pneumoniae infections with strains harboring both genes encoding ESBLs and the armA 16S rRNA methyltransferase gene.…”