Abstract
Invasive syndrome caused by Klebsiella pneumoniae (KP), including liver abscess, is mainly caused by communityacquired strains with characteristics of positive hypermucoviscosity (HV) phenotype and regulator of mucoid phenotype A (rmpA) and transcriptional activator (rmpA2) genes. Extended-spectrum b-lactamase-producing KP (ESBLKP) is commonly nosocomial and rarely HV-positive. We aimed to explore the reasons of the rarer prevalence of HV phenotype, rmpA and rmpA2 as well as the virulence phenotype among the ESBL-KP isolates from clinical specimens than those non-ESBL isolates. The β-lactamase genes, rmpA, rmpA2 and genes for K capsule serotype of 440 KP isolates were analyzed. The virulence of the isolates was characterized by the mouse lethality experiments. The prevalence rates of HV phenotype (~50% vs. <10%) as well as rmpA and rmpA2 genes (~50-60% vs. <20-30%) were significantly higher in non-ESBL group than in the ESBL group (p <0.0001). Expression of HV phenotype in the rmpA-positive KP isolates was significantly rarer in the ESBL group than in non-ESBL group (33.3% vs. 91.9%, p <0.0001). The frameshift mutations of rmpA and/or rmpA2 corresponded to negative HV phenotype of KP isolates that harbored the rmpA and?or rmpA2, resulting in variable mouse lethality (LD50, ~103->5 × 107CFU). The mutation rates might significantly differ among KP isolates from various sources. Virulence was dependent on rmpA-related HV phenotype. In conclusion, ESBL-KP isolates were less hypermucoviscous and less virulent than non-ESBL KP isolates, mostly due to concurrently lower carriage and higher mutation rates of the rmpA and rmpA2 genes.
| Original language | English |
|---|---|
| Pages (from-to) | 162-172 |
| Number of pages | 11 |
| Journal | Virulence |
| Volume | 6 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Apr 1 2015 |
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Keywords
- ESBL hypermucoviscosity
- Klebsiella pneumoniae
- RmpA gene
- Spontaneous mutation
ASJC Scopus subject areas
- Infectious Diseases
- Microbiology
- Parasitology
- Immunology
- Microbiology (medical)
Cite this
Low prevalence of rmpA and high tendency of rmpA mutation correspond to low virulence of extended spectrum β-lactamase-producing klebsiella pneumoniae isolates. / Yu, Wen Liang; Lee, Mei Feng; Tang, Hung Jen; Chang, Ming Chung; Chuang, Yin Ching.
In: Virulence, Vol. 6, No. 2, 01.04.2015, p. 162-172.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Low prevalence of rmpA and high tendency of rmpA mutation correspond to low virulence of extended spectrum β-lactamase-producing klebsiella pneumoniae isolates
AU - Yu, Wen Liang
AU - Lee, Mei Feng
AU - Tang, Hung Jen
AU - Chang, Ming Chung
AU - Chuang, Yin Ching
PY - 2015/4/1
Y1 - 2015/4/1
N2 - Invasive syndrome caused by Klebsiella pneumoniae (KP), including liver abscess, is mainly caused by communityacquired strains with characteristics of positive hypermucoviscosity (HV) phenotype and regulator of mucoid phenotype A (rmpA) and transcriptional activator (rmpA2) genes. Extended-spectrum b-lactamase-producing KP (ESBLKP) is commonly nosocomial and rarely HV-positive. We aimed to explore the reasons of the rarer prevalence of HV phenotype, rmpA and rmpA2 as well as the virulence phenotype among the ESBL-KP isolates from clinical specimens than those non-ESBL isolates. The β-lactamase genes, rmpA, rmpA2 and genes for K capsule serotype of 440 KP isolates were analyzed. The virulence of the isolates was characterized by the mouse lethality experiments. The prevalence rates of HV phenotype (~50% vs. <10%) as well as rmpA and rmpA2 genes (~50-60% vs. <20-30%) were significantly higher in non-ESBL group than in the ESBL group (p <0.0001). Expression of HV phenotype in the rmpA-positive KP isolates was significantly rarer in the ESBL group than in non-ESBL group (33.3% vs. 91.9%, p <0.0001). The frameshift mutations of rmpA and/or rmpA2 corresponded to negative HV phenotype of KP isolates that harbored the rmpA and?or rmpA2, resulting in variable mouse lethality (LD50, ~103->5 × 107CFU). The mutation rates might significantly differ among KP isolates from various sources. Virulence was dependent on rmpA-related HV phenotype. In conclusion, ESBL-KP isolates were less hypermucoviscous and less virulent than non-ESBL KP isolates, mostly due to concurrently lower carriage and higher mutation rates of the rmpA and rmpA2 genes.
AB - Invasive syndrome caused by Klebsiella pneumoniae (KP), including liver abscess, is mainly caused by communityacquired strains with characteristics of positive hypermucoviscosity (HV) phenotype and regulator of mucoid phenotype A (rmpA) and transcriptional activator (rmpA2) genes. Extended-spectrum b-lactamase-producing KP (ESBLKP) is commonly nosocomial and rarely HV-positive. We aimed to explore the reasons of the rarer prevalence of HV phenotype, rmpA and rmpA2 as well as the virulence phenotype among the ESBL-KP isolates from clinical specimens than those non-ESBL isolates. The β-lactamase genes, rmpA, rmpA2 and genes for K capsule serotype of 440 KP isolates were analyzed. The virulence of the isolates was characterized by the mouse lethality experiments. The prevalence rates of HV phenotype (~50% vs. <10%) as well as rmpA and rmpA2 genes (~50-60% vs. <20-30%) were significantly higher in non-ESBL group than in the ESBL group (p <0.0001). Expression of HV phenotype in the rmpA-positive KP isolates was significantly rarer in the ESBL group than in non-ESBL group (33.3% vs. 91.9%, p <0.0001). The frameshift mutations of rmpA and/or rmpA2 corresponded to negative HV phenotype of KP isolates that harbored the rmpA and?or rmpA2, resulting in variable mouse lethality (LD50, ~103->5 × 107CFU). The mutation rates might significantly differ among KP isolates from various sources. Virulence was dependent on rmpA-related HV phenotype. In conclusion, ESBL-KP isolates were less hypermucoviscous and less virulent than non-ESBL KP isolates, mostly due to concurrently lower carriage and higher mutation rates of the rmpA and rmpA2 genes.
KW - ESBL hypermucoviscosity
KW - Klebsiella pneumoniae
KW - RmpA gene
KW - Spontaneous mutation
UR - http://www.scopus.com/inward/record.url?scp=84926664369&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84926664369&partnerID=8YFLogxK
U2 - 10.1080/21505594.2015.1016703
DO - 10.1080/21505594.2015.1016703
M3 - Article
C2 - 25830726
AN - SCOPUS:84926664369
VL - 6
SP - 162
EP - 172
JO - Virulence
JF - Virulence
SN - 2150-5594
IS - 2
ER -