A comparison of 2-year Kaplan–Meier survival curves of PLA patients with and without septic ocular or CNS complications (p = 0.502, by log-rank test).

<p>A comparison of 2-year Kaplan–Meier survival curves of PLA patients with and without septic ocular or CNS complications (p = 0.502, by log-rank test).</p

Clinical characteristics of PLA patients with and without septic ocular or central nervous system complications.

<p><b>NOTE.</b> PLA, pyogenic liver abscess.</p

A comparison of 2-year Kaplan–Meier survival curves of PLA patients aged <65 years and a Charlson comorbidity index ≤1 (i.e. between 0 and 1) with and without septic ocular or CNS complications (p = 0.001, by log-rank test).

<p>A comparison of 2-year Kaplan–Meier survival curves of PLA patients aged <65 years and a Charlson comorbidity index ≤1 (i.e. between 0 and 1) with and without septic ocular or CNS complications (p = 0.001, by log-rank test).</p

The frequency of PLA cases with septic ocular or central nervous system complications.

<p><b>NOTE.</b> PLA, pyogenic liver abscess.</p

Single or in Combination Antimicrobial Resistance Mechanisms of <i>Klebsiella pneumoniae</i> Contribute to Varied Susceptibility to Different Carbapenems

<div><p>Resistance to carbapenems has been documented by the production of carbapenemase or the loss of porins combined with extended-spectrum β-lactamases or AmpC β-lactamases. However, no complete comparisons have been made regarding the contributions of each resistance mechanism towards carbapenem resistance. In this study, we genetically engineered mutants of <i>Klebsiella pneumoniae</i> with individual and combined resistance mechanisms, and then compared each resistance mechanism in response to ertapenem, imipenem, meropenem, doripenem and other antibiotics. Among the four studied carbapenems, ertapenem was the least active against the loss of porins, cephalosporinases and carbapenemases. In addition to the production of KPC-2 or NDM-1 alone, resistance to all four carbapenems could also be conferred by the loss of two major porins, OmpK35 and OmpK36, combined with CTX-M-15 or DHA-1 with its regulator AmpR. Because the loss of OmpK35/36 alone or the loss of a single porin combined with <i>bla</i>_CTX-M-15 or <i>bla</i>_DHA-1-<i>ampR</i> expression was only sufficient for ertapenem resistance, our results suggest that carbapenems other than ertapenem should still be effective against these strains and laboratory testing for non-susceptibility to other carbapenems should improve the accurate identification of these isolates.</p> </div

Comparison of the bactericidal activity of normal human serum (NHS) with different treatments against serum-susceptible <i>K. pneumoniae</i> mutants.

a<p>NHSMgEGTA, NHS plus inhibition of the classical and lectin complement pathways; NHS50°C, NHS with inhibition of the alternative complement pathway. NHS was decomplemented via heating at 56°C for 30 min.</p>b<p>Percent survival of cells after 3 h of serum contact. Each value represents the means of three independent experiments ± the standard deviation. Boldface numbers indicate a significant (<i>P</i><0.05) difference in survival rate compared with the same strain incubated in 75% NHS.</p><p>Comparison of the bactericidal activity of normal human serum (NHS) with different treatments against serum-susceptible <i>K. pneumoniae</i> mutants.</p

Distribution of serum-sensitive and serum-resistant serotypes of <i>K. pneumoniae</i> selected for this study.

<p>*The 17 strains of non-K1/K2 contained one isolate each of K3, K6, K15, K16, K17, K20, K21, K22, K29, K31, K36, K38, and K54 and two isolates each of K55 and K28. The grading system used to assess serum resistance was described by Podschun et al. (1991).</p

A Suitable Streptomycin-Resistant Mutant for Constructing Unmarked In-Frame Gene Deletions Using <i>rpsL</i> as a Counter-Selection Marker

<div><p>The streptomycin counter-selection system is a useful tool for constructing unmarked in-frame gene deletions, which is a fundamental approach to study bacteria and their pathogenicity at the molecular level. A prerequisite for this system is acquiring a streptomycin-resistant strain due to <i>rpsL</i> mutations, which encodes the ribosomal protein S12. However, in this study no streptomycin resistance was found to be caused by <i>rpsL</i> mutations in all 127 clinical strains of <i>Klebsiella pneumoniae</i> isolated from liver abscess patients. By screening 107 spontaneous mutants of streptomycin resistance from a clinical strain of <i>K. pneumoniae</i>, nucleotide substitution or insertion located within the <i>rpsL</i> was detected in each of these strains. Thirteen different mutants with varied S12 proteins were obtained, including nine streptomycin-dependent mutants. The virulence of all four streptomycin-resistant mutants was further evaluated. Compared with the parental strain, the K42N, K42T and K87R mutants showed a reduction in growth rate, and the K42N and K42T mutants became susceptible to normal human serum. In the mice LD₅₀ (the bacterial dose that caused 50% death) assay, the K42N and K42T mutants were ∼1,000-fold less lethal (∼2×10⁵ CFU) and the K87R mutant was ∼50-fold less lethal (∼1×10⁴ CFU) than the parental strain (∼2×10² CFU). A K42R mutant showed non-observable effects on the above assays, while this mutant exhibited a small cost (<i>P</i><0.01) in an <i>in vitro</i> growth competition experiment. In summary, most of the <i>K. pneumoniae</i> strains with streptomycin resistance caused by <i>rpsL</i> mutations are less virulent than their parental strain in the absence of streptomycin. The K42R mutant showed similar pathogenicity to its parental strain and should be one of the best choices when using <i>rpsL</i> as a counter-selection marker.</p></div

The rate at which neutrophils from 11 healthy volunteers killed serotypes K1 and K6 <i>K. pneumoniae</i>.

<p>The percentage of killing is expressed as the mean ± SD and calculated as the total number of bacteria killed divided by the number of viable bacteria in the initial inoculum. K1 vs. K6: <i>p</i><0.01 (n = 3 for each).</p

Pathologic features of abscesses due to serotypes K1 and K6 <i>K. pneumoniae</i> in different mouse tissues.

<p>(A). Necrosis can be seen in the liver and at metastatic infection sites in mice injected with K1 <i>K. pneumoniae</i>. No inflammation was seen in the liver of mice injected with serotype K6. (B). Inflammation was not found in the lungs, spleen, or kidneys of mice injected with serotypes K1 and K6.</p