A compressed logistic equation on bacteria growth: inferring time-dependent growth rate.

We propose a compressed logistic model for bacterial growth by invoking a time-dependent rate instead of the intrinsic growth rate (constant), which was adopted in traditional logistic models. The new model may have a better physiological basis than the traditional ones, and it replicates experimental observations, such as the case example forE. coli, Salmonella,andStaphylococcus aureus. Stochastic colonial growth at a different rate may have a fractal-like nature, which should be an origin of the time-dependent reaction rate. The present model, from a stochastic viewpoint, is approximated as a Gaussian time evolution of bacteria (error function).

Laboratory surveillance of antimicrobial resistance and multidrug resistance among Streptococcus pneumoniae isolated in the Kinki region of Japan, 2001-2015.

The 7-valent pneumococcal conjugate vaccine (PCV7) was introduced among children in Japan in 2010. There are no long-term multicenter surveillance studies of antimicrobial resistance in S. pneumoniae before and after the introduction of PCV7. Therefore, we examined chronological trends in antimicrobial resistance among 4534 strains of S. pneumoniae isolated from both children and adults in the Kinki region of Japan during 2001-2015. High-level penicillin and third-generation cephalosporin resistance in S. pneumoniae increased among both children and adults during the period before the introduction of PCV7 (2001-2010). Besides penicillin and cephalosporin, pneumococcal carbapenem and macrolide resistance increased among children. The rate of resistance to these antibiotics was higher among children than among adults. The introduction of PCV7 decreased the rate of non-susceptibility to ß-lactam antibiotics and the rate of multidrug resistant S. pneumoniae among children, but not among adults.

[Relationship between time taken from collection of blood to incubation and measurement in whole-blood interferon gamma assay for diagnosis of Mycobacterium tuberculosis infection].

BACKGROUND: The introduction of second-generation QuantiFERON-TB (QFT) enables the diagnosis of Mycobacterium tuberculosis (TB) infection with high specificity and sensitivity. This in vitro diagnostic test uses 2 TB-specific proteins (ESAT-6 and CFP-10) to stimulate cells in heparinized whole blood and detects interferon-gamma (IFN-gamma) produced from blood cells. When QFT is done in laboratories outside of the hospital, several hours may be required to transport blood samples. We studied the relationship between QFT results and the time taken from collection of blood to incubation (preincubation time). METHODS: Heparinized whole blood drawn from TB suspects was immediately transported to a laboratory. We started to incubate 4 aliquots of blood with ESAT-6, CFP-10, mitogen (phytohemagglutinin), and nil control, at 1, 3, 6, 9, and 12 h after blood was drawn. After incubation, the concentration of IFN-gamma in each plasma sample was determined by ELISA, and values E and C were expressed as the concentration of IFN-gamma with ESAT-6 or CFP-10, minus the concentration of IFN-gamma in the nil control. Value E or C > or =0.35IU/mL was considered positive, > or =0.10 and<0.35IU/mL as equivocal (gray zone), and<0.10IU/mL as negative. We analyzed 8 patients with value E or C > or =0.10IU/mL at a preincubation time of 1 h. RESULTS: Value E and C decreased especially for preincubation time >6 h. As a result, the interpretation of value E changed from "positive" to "equivocal" in 2 cases and from "equivocal" to "negative" in 2 cases. Interpretation of value C also changed from "positive" to "equivocal" or "negative" in 2 cases and from "equivocal "to "negative" in 1 case. Even if the higher of value E or C were used for analysis, QFT results changed in half of patients when preincubation time was>6 h. CONCLUSION: Since QFT results in half of patients changed when preincubation time was>6 h, incubation of whole blood should start < or =6 h after blood drawing.

[In vitro activity of antimicrobial agents against clinical isolates of Pseudomonas aeruginosa].

Two hundred and seven clinical isolates of Pseudomonas aeruginosa were collected at Tenri Hospital between April 2003 and March 2004. We determined the minimum inhibitory concentration (MIC) of 16 antimicrobial agents, including prulifloxacin, pazufloxacin and biapenem which were recently published in Japan, against these isolates according to the guidelines of the Clinical and Laboratory Standards Institute. For the fluoroquinolones, the rank order of activity was prulifloxacin (MIC50, 0.5 microg/ml)>ciprofloxacin (1 microg/ml)> pazufloxacin (2 microg/ml)=levofloxacin (2 microg/ml)>gatifloxacin (4 microg/ml). For the carbapenems, the rank order of activity was meropenem (MIC50, 1 microg/ml)=biapenem (1 microg/ml)>imipenem (2 microg/m)>panipenem (8 microg/ml). For the cephalosporins and monobactam, the overall rank order of activity was cefozopran (MIC50, 4 microg/ml)= ceftazidime (4 microg/ml)>cefepime (8 microg/ml)=piperacillin/tazobactam (8 microg/ml)>aztreonam (16 microg/ml)= cefoperazone/sulbactam (16 microg/ml)=cefpirome (16 microg/ml). The rates of susceptibility to antimicrobial agents as per the criteria of the Japanese Society of Antimicrobial Chemotherapy were especially high for cefozopran (63%), biapenem and meropenem (61%), and pazufloxacin (53%) and ciprofloxacin (53%). These findings suggest that prulifloxacin, pazufloxacin and biapenem, which are newly introduced, are clinically effective in the treatment of infection caused with P. aeruginosa.

[Surveillance of antimicrobial resistance of Streptococcus pneumoniae isolates from the Kinki Region of Japan during 2003/2004. The Surveillance Program of Bacterial Resistance in the Kinki Region of Japan; SBRK].

Three hundred seventy five isolates of Streptococcus pneumoniae were collected from 14 medical institutions in the Kinki region of Japan between November 2003 and February 2004. We determined the minimum inhibitory concentration (MIC) of penicillin G (PCG) and 25 of other antimicrobial agents against these isolates according to the National Committee for Clinical Laboratory Standards (NCCLS). Overall, 71.5% of all isolates were resistant to PCG (intermediate and resistant categories were 51.7% and 19.8%, respectively). For the carbapenems and penem, the rank order of activity was PAPM (MIC90, 0.12 microg/ml) > IPM (0.25 microg/ml) > MEPM (0.5 microg/ml) = FRPM (0.5 microg/ml). For the cephems, the overall rank order of activity was CPR (MIC90, 0.5 microg/ml) = CDTR (0.5 microg/ml) > CTRX (1 microg/ml) = CTX (1 microg/ml) = CZOP (1 microg/ml) = CFPN (1 microg/ml). Rank order activity for six of fluoroquinolones was TFLX = MFLX (MIC90, 0.25 microg/ml) > GFLX (0.5 microg/ ml) = SPFX (0.5 microg/ml) > LVFX (1 microg/ml) > PZFX (4 microg/ml). The rate of resistance to fluoroquinolones per the NCCLS criteria were very low, ranging from 0.7% to 2.6%. Rate of resistance to other antimicrobiotics were CAM, 77.0%; CLDM, 41.7%; TEL, 0%; VCM, 0%; ST, 32.7%, and CP, 21.4%.

[Resistance to antimicrobiotics and mutation of PBPs in Streptococcus pneumoniae isolated from Kinki region of Japan].

We studied the susceptibility to penicillin G (PCG) and other antimicrobiotics in 235 clinical isolates of Streptococcus pneumoniae. Samples were collected between April 1 and June 30, 2000 from nine medical institutions of the Kinki Region of Japan. We classified the minimum inhibitory concentration (MIC) of PCG according to the National Committee for Clinical Laboratory Standards (NCCLS) criteria. The overall rate of all types of S. pneumoniae resistance was 53.2% (penicillin-susceptible S. pneumoniae (PSSP): 46.8%, penicillin-intermediate S. pneumoniae (PISP): 42.6%, penicillin-resistant S. pneumoniae (PRSP): 10.6%). In other antimicrobiotics, the resistance (R)/intermediate susceptibility (I) rates (R/I%) were as follows: ceftriaxone, 28.9%; cefotaxime, 7.7%; imipenem, 8.9%; meropenem, 9.8%; clarithromycin, 82.6%; clindamycin, 42.1%; levofloxacin, 0.4%; vancomycin, 0%. We used the polymerase chain reaction to study the mutations of the penicillin-binding proteins pbp1 a, pbp2b, and pbp2x in 140 strains of S. pneumoniae in the MIC for PCG was < 0.5 microgram/ml. Among the 109 strains of PSSP, 32 (29.4%) had no mutation and 77 (70.6%) showed mutation of more than one of the pbp mutations. Among the 31 strains of PISP, only 1 strain (3.2%) was not mutated. Since 70.6% of the strains classified as PSSP had pbp mutations, S. pneumoniae clearly can acquire resistance to anti-microbiotics. In the future, a comprehensive surveillance of S. pneumoniae is necessary.

In vitro activity of beta-lactams and quinolones against AmpC beta-lactamase-producing Escherichia coli.

We studied the antimicrobial susceptibility of AmpC beta-lactamase-producing Escherichia coli isolates collected at ten medical institutions in the Kinki area of Japan during a 6-month period (November 2002 through April 2003). Of 2845 E. coli isolates tested, 29 (1.0%) showed a minimum inhibitory concentration (MIC) for cefazolin of more than 8 microg/ml and were three-dimensional extract test positive. In standard inoculum susceptibility tests against these 29 strains, the MIC90s for the four carbapenems tested ranged from 0.06 microg/ml to 0.5 microg/ml, and these compounds were more active than the other beta-lactams, with meropenem being the most active. The MIC90s for beta-lactams, except carbapenems, ranged from 4 microg/ml to 32 microg/ml, with cefepime being the most active. In high inoculum susceptibility tests against these strains, the MIC90s for the four carbapenems and cefepime were 8 microg/ml or less, and these compounds were more active than other beta-lactams. The MIC90s for beta-lactams, except carbapenems and cefepime, were 32 microg/ml or more. The MIC90s for the five quinolones tested ranged from 4 microg/ml to 16 microg/ml, and the order of increasing susceptibility was ciprofloxacin > levofloxacin, gatifloxacin and pazufloxacin > prulifloxacin.

Production of CTX-M-3 extended-spectrum beta-lactamase and IMP-1 metallo beta-lactamase by five Gram-negative bacilli: survey of clinical isolates from seven laboratories collected in 1998 and 2000, in the Kinki region of Japan.

The aim of this study was to research the distribution in the Kinki region of Japan of Enterobacteriaceae and Pseudomonas aeruginosa that produce extended-spectrum beta-lactamase (ESBL) and metallo beta-lactamase (MBL). One thousand isolates, 200 of each of four enterobacterial species (i.e. Escherichia coli, Klebsiella pneumoniae, Enterobacter cloacae and Serratia marcescens) and 200 of P. aeruginosa, were collected from seven different laboratories during two 2 month periods, one in 1998 and one in 2000. A double-disc synergy test (DDST) and 2-mercaptopropionic acid inhibition test (2-MPAT) were used to confirm beta-lactamase-producing isolates. The DDST was positive for one isolate of E. coli, five of K. pneumoniae, two of E. cloacae and 14 of S. marcescens. The 2-MPAT was positive for five isolates of S. marcescens and two of P. aeruginosa. We identified the beta-lactamase type of each isolate by molecular confirmatory tests (isoelectric focusing, PCR and DNA sequencing): CTX-M-3 ESBLs (three isolates of K. pneumoniae, two of E. cloacae and 13 of S. marcescens), CTX-M-2 ESBL (one isolate of K. pneumoniae), SHV-12 ESBLs (one isolate of E. coli and one of S. marcescens), CTX-M-3 and SHV-12 combination ESBL (one isolate of K. pneumoniae) and IMP-1 MBLs (five isolates of S. marcescens and two of P. aeruginosa). In conclusion, many species of Gram-negative bacilli that produce CTX-M-3 ESBLs and IMP-1 MBLs were disseminated widely in different hospitals of the Kinki region of Japan. Therefore, monitoring of laboratory bacterial ecology seems important to stop the spread of these strains through nosocomial outbreaks.