Prevention of 5-fluorouracil-induced infection with indigenous Escherichia coli in tumor-bearing mice by nonspecific immunostimulation

1992 ◽  
Vol 38 (8) ◽  
pp. 774-778 ◽  
Author(s):  
Koji Nomoto ◽  
Teruo Yokokura ◽  
Kikuo Nomoto

We have previously reported that the lethal toxicity of 5-fluorouracil (5-FU) in specific-pathogen-free mice is due to an indigenous infection with Escherichia coli (K. Nomoto, T. Yokokura, Y. Yoshikai, et al. Can. J. Microbiol. 37: 244–247, 1991). In the present study, we demonstrate that nonspecific immunostimulation augments host resistance against the lethal toxicity of 5-FU in tumor-bearing mice. Intravenous administration of a preparation of heat-killed Lactobacillus casei (LC 9018), a nonspecific immunostimulant, at a dose of 20 mg/kg to BALB/c mice augmented their resistance against the lethal toxicity of 5-FU if the preparation was injected into the mice 10–40 days before administration of 5-FU. Injection of LC 9018 into BALB/c mice bearing Meth A fibrosarcoma also enhanced their resistance against the lethality of 5-FU. Systemic infection with E. coli was induced in all of the 5-FU-treated tumor-bearing mice 10 days or more after administration of the drug at a lethal dose of 500 mg/kg, and it was accompanied by an overgrowth of the bacteria in the intestine. Treatment of tumor-bearing mice with LC 9018 resulted in decreased rates of occurrence of systemic infection with E. coli and inhibition of overgrowth of the bacteria in the intestine after administration of 5-FU. A single administration of either LC 9018 or 5-FU significantly inhibited the growth of Meth A cells in vivo, and a combined antitumor effect was shown in the mice treated with both 5-FU and LC 9018. Key words: tumor-bearing mice, fluorouracil, nonspecific immunostimulation, indigenous infection, Escherichia coli.

2018 ◽  
Vol 73 (6) ◽  
pp. 1579-1585 ◽  
Author(s):  
M Giles ◽  
S A Cawthraw ◽  
M AbuOun ◽  
C M Thomas ◽  
D Munera ◽  
...  

AbstractObjectivesTo assess stability and contribution of a large ESBL-encoding IncI1 plasmid to intestinal colonization by Escherichia coli O104:H4 in two different mammalian hosts.MethodsSpecific-pathogen-free 3–4-day-old New Zealand White rabbits and conventionally reared 6-week-old weaned lambs were orally infected with WT E. coli O104:H4 or the ESBL-plasmid-cured derivative, and the recovery of bacteria in intestinal homogenates and faeces monitored over time.ResultsCarriage of the ESBL plasmid had differing impacts on E. coli O104:H4 colonization of the two experimental hosts. The plasmid-cured strain was recovered at significantly higher levels than WT during late-stage colonization of rabbits, but at lower levels than WT in sheep. Regardless of the animal host, the ESBL plasmid was stably maintained in virtually all in vivo passaged bacteria that were examined.ConclusionsThese findings suggest that carriage of ESBL plasmids has distinct effects on the host bacterium depending upon the animal species it encounters and demonstrates that, as for E. coli O157:H7, ruminants could represent a potential transmission reservoir.


1991 ◽  
Vol 37 (3) ◽  
pp. 244-247 ◽  
Author(s):  
Koji Nomoto ◽  
Teruo Yokokura ◽  
Yasunobu Yoshikai ◽  
Masao Mitsuyama ◽  
Kikuo Nomoto

A single administration of fluorouracil (5-FU), a well-used cancer chemotherapeutic agent, at high doses (338–800 mg/kg) to specific pathogen free mice induced a lethal infection with Escherichia coli. The infection was manifested in all the mice treated with 5-FU 7–14 days after administration of the drug, when the number of E. coli in liver reached levels ranging from 108 to 1010 colony-forming units, and the type of the infecting bacteria was limited to E. coli. The infection was accompanied with the increase in the population levels of E. coli in the intestinal tract which reached levels about 103 to 104 times as high as those of normal mice. Administration of tegafur, a less toxic derivative of 5-FU, to mice at a lethal dose of 1280 mg/kg induced infection with E. coli similar to that induced by 5-FU. Multiple administration of both streptomycin sulfate and cephalothin to mice after treatment with 5-FU protected the mice completely from the lethal infection induced by 5-FU, suggesting that the lethality of 5-FU was due to the indigenous bacterial infection. Key words: fluorouracil, Escherichia coli, mice, indigenous infection.


1980 ◽  
Vol 29 (3) ◽  
pp. 1073-1081
Author(s):  
Rodney D. Berg

Escherichia coli C25 maintained population levels of 10 9 to 10 10 per g of cecum and translocated to 100% of the middle mesenteric lymph nodes in gnotobiotic mice monoassociated with E. coli C25. Intragastric inoculation of these mice with the cecal contents from specific-pathogen-free mice reduced the population levels of E. coli C25 to 10 6 per g of cecum and completely inhibited translocation to the mesenteric lymph nodes. Intragastric inoculation with heat-treated, Formalintreated, or filtered cecal contents did not reduce the population levels of E. coli C25 or reduce the incidence of translocation of E. coli C25 to the mesenteric lymph nodes. Thus, viable bacteria apparently are required in the cecal contents inocula to reduce the population levels and the incidence of translocation of E. coli C25. Treatment with streptomycin plus bacitracin decreased the anaerobic bacterial levels in these gnotobiotic mice, allowing increased population levels of E. coli C25 and increased translocation to the mesenteric lymph nodes. E. coli C25 also translocated to the mesenteric lymph nodes of specific-pathogen-free mice treated with streptomycin and bacitracin before colonization with E. coli C25. The high cecal population levels of E. coli C25 in these antibiotic-decontaminated specific-pathogen-free mice apparently overwhelm any barrier to translocation exerted by the immunologically developed lamina propria of the specific-pathogen-free mice. Inoculation of gnotobiotic mice with a cecal flora also reduced the population levels of an indigenous strain of E. coli with a concomitant inhibition of translocation of the indigenous E. coli to the mesenteric lymph nodes. Thus, bacterial antagonism of the gastrointestinal population levels of certain indigenous bacteria, such as E. coli , by other members of the normal bacterial flora appears to be an important defense mechanism confining bacteria to the gastrointestinal tract.


2020 ◽  
Vol 38 (1) ◽  
pp. 61
Author(s):  
Sruti Listra Adrenalin ◽  
Lynda Nugrahaning Imanjati ◽  
Ima Fauziah ◽  
Vinsa Cantya Prakasita ◽  
Sitarina Widyarini ◽  
...  

Avian pathogenic Escherichia coli (APEC) is a cause of colibacillosis in poultry, one of the respiratory disease that causes serious problems in the poultry industry. The APEC can cause high mortality and culling, decreased production, and high costs of treatment. Manifestations of colibacillosis are airsacculitis, perihepatitis, and pericarditis. The APEC serotypes that are widely identified in the field are O1K1, O2K1, and O78K80. Embryo lethality assay (ELA) is a method for determine the virulence of APEC serotypes. The aim of this study was to determine the virulence characteristic of APEC isolates. Five APEC serotypes O1K1, O2K1, O78K80, O157H7, and unknown serotype were used for ELA method by inoculated E. coli into chorioallantoic of specific pathogen free 12-days old embryos. Each group of 10 embryos, inoculated E. coli dose of 100-500 CFU/ 0,1 ml. Candling was carried out for 6 days (18-days old embryo) to determined the mortality and pathological lesions. The percentage of embryo mortality post-inoculated with APEC O1K1, O2K1, unknown serotypes were 100% (10/10), O78K80 serotype was 90% (9/10), and O157H7 serotype was 70% (70%). Lesions of all embryos were cranial and extremity hemorrhage. In this study, E. coli isolates had high virulence. 


Author(s):  
Henry Jurado-Gámez ◽  
Manuel Gúzman-Insuasty

<p>Se determinó la cinética, pruebas de crecimiento y el efecto de inhibición <em>in vitro</em> de <em>Lactobacillus casei</em> sobre <em>Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus agalactiae </em>y<em> Escherichia coli</em>. Se usaron cepas de casa comercial y cepas aisladas en la Vereda La Victoria, Corregimiento de Catambuco al suroccidente del municipio de Pasto, Nariño, Colombia. Se evaluó el efecto de los antibióticos Dicloxacilina, Cefepima, Cefalotina, Ciprofloxacina, Gentamicina, Penicilina, Trimetropim Sulfa y Ampicilina. Se evaluó la inhibición producida por <em>L. casei</em> y su sobrenadante sobre las bacterias patógenas. El crecimiento de la bacteria láctica se evaluó con tres niveles de pH (2,5, 4,5 y 7),  tres concentraciones de sales biliares (0,5, 1 y 2%) y dos de bilis bovina (1 y 1,2%), y dos temperaturas (38 y 45°C). Igualmente se determinó la cinética de crecimiento y las variables pH, azúcar total, proteína y ácido láctico.  Mediante HPLC se determinaron los péptidos y los ácidos orgánicos presentes en el sobrenadante. <em>L. casei </em>mostró susceptibilidad a la Ciprofloxacina y Ampicilina, mientras que <em>S. aureus </em>mostró susceptibilidad y resistencia a todos los antibióticos para la cepa comercial y aislada respectivamente, el mismo comportamiento se presentó con <em>S. epidermidis</em>. Las cepas de <em>S. agalactiae</em> y <em>E. coli</em> aisladas y comerciales mostraron susceptibilidad a los antibióticos.  La cepa láctica mostró un efecto de inhibición de <em>S. aureus</em>, <em>S. epidermidis</em> y  <em>S. agalactiae</em>, pero no fue efectiva con <em>E. coli</em>, igual comportamiento se observó con el uso del sobrenadante de la bacteria láctica. Se encontró crecimiento de 1 x 10<sup>10</sup> y 5,1 x 10<sup>7</sup> UFC/ml para 1 y 1,2 % de bilis bovina; 2,3 x 10<sup>7</sup>, 1 x 10<sup>9</sup> y 3 x 10<sup>8</sup> UFC/ml para 0,5, 1 y 2 % de sales biliares respectivamente; 1,1 x 10<sup>11</sup>, 2,0 x 10<sup>10</sup> y 1,0 x 10<sup>10</sup> UFC/ml para  pH de 2,5, 4,5 y 7 respectivamente. La fase exponencial se encontró a 16:48 horas con un crecimiento de 3 x 10<sup>10</sup> UFC/ml. La variables pH, azúcar, acidez y proteína durante la fase exponencial fueron de 4,94, 0,88 mg/l, 2,89 mg/l y 1,9 mg/l, respectivamente. La prueba de HPLC para péptidos mostró la presencia de una cadena VAL-TIR-VAL y para ácidos orgánicos se encontró una producción de 83,46% de ácido láctico. <em>L. casei </em> mostró buenas características probiótica que permitirían su aplicación en ensayos in vivo para el control de microorganismos causantes de mastitis subclínica en vacas.</p>


2005 ◽  
Vol 73 (3) ◽  
pp. 1836-1846 ◽  
Author(s):  
Angus Best ◽  
Roberto M. La Ragione ◽  
A. Robin Sayers ◽  
Martin J. Woodward

ABSTRACT Shiga toxin (Stx)-positive Escherichia coli O157:H7 readily colonize and persist in specific-pathogen-free (SPF) chicks, and we have shown that an Stx-negative E. coli O157:H7 isolate (NCTC12900) readily colonizes SPF chicks for up to 169 days after oral inoculation at 1 day of age. However, the role of intimin in the persistent colonization of poultry remains unclear. Thus, to investigate the role of intimin and flagella, which is a known factor in the persistence of non-O157 E. coli in poultry, isogenic single- and double-intimin and aflagellar mutants were constructed in E. coli O157:H7 isolate NCTC12900. These mutants were used to inoculate (105 CFU) 1-day-old SPF chicks. In general, significant attenuation of the aflagellate and intimin-aflagellate mutants, but not the intimin mutant, was noted at similar time points between 22 and 92 days after inoculation. The intimin-deficient mutant was still being shed at the end of the experiment, which was 211 days after inoculation, 84 days more than the wild type. Shedding of the aflagellar and intimin-aflagellar mutants ceased 99 and 113 days after inoculation, respectively. Histological analysis of gastrointestinal tissues from inoculated birds gave no evidence for true microcolony formation by NCTC12900 or intimin and aflagellar mutants to epithelial cells. However, NCTC12900 mutant derivatives associated with the mucosa were observed as individual cells and/or as large aggregates. Association with luminal contents was also noted. These data suggest that O157 organisms do not require intimin for the persistent colonization of chickens, whereas flagella do play a role in this process.


2016 ◽  
Vol 30 (1-2) ◽  
pp. 31-38
Author(s):  
Fahareen Binta Mosharraf ◽  
Chowdhury Rafiqul Ahsan ◽  
Jamalun Nessa ◽  
Mahmuda Yasmin

Escherichia coli O157:H7 is a newly emerged pathogen, which has been recognized as a major cause of large scale epidemics and thousands of sporadic cases of gastrointestinal illness. This observation particularly calls for the in vivo examination of E. coli O157 candidates in an attempt to mimic various aspects of E. coli O157:H7 disease symptoms in humans. Healthy conventional Swiss albino mice were used for investigating the clinical manifestation exerted by stx1A and stx2A positive E. coli O157:H7 in various doses applied through three alternative routes (oral, intramuscular and intraperitoneal). The highest titer of orally added E. coli 0157:H7 (109 CFU ml-1) among the five test doses had started symptoms at the earliest time and manifested most of the classical symptoms. The symptoms started to become visible at 14th hour, increased with time and had reached moribund condition near 48th hour just before death of the host. The oral way of E. coli O157:H7 addition at the dose of 100 ?l suspension containing 1 X 109CFU ml-1 was taken as the most potent concentration in producing bacterial fatality and hence was selected as the Minimum Lethal Dose (MLD).Bangladesh J Microbiol, Volume 30, Number 1-2,June-Dec 2013, pp 31-38


1986 ◽  
Vol 23 (6) ◽  
pp. 712-717 ◽  
Author(s):  
K. Nakamura ◽  
Y. Imada ◽  
M. Maeda

Specific-pathogen-free 10-week-old chickens were inoculated via the air sac with Escherichia coli and showed lymphocytic depletion of bursa of Fabricius and thymus. In experiment I, chickens were necropsied at 12 and 24 hours, 2, 3, and 5 days after inoculation. At 12 hours after inoculation there was lymphocytic depletion in the medulla of lymphoid follicles of the bursa. At 24 hours after inoculation there was lymphocytic depletion also in the cortex of follicles and edema in interfollicular interstitium and follicular medulla. At 2 and 3 days after inoculation there were more marked lymphocytic depletion in medulla and cortex, and fibrosis in interfollicular interstitium. Partial repopulation of follicles with lymphocytes was seen at 5 days after inoculation. In the thymus, lymphocytic depletion occurred in the cortex. At 12 hours after inoculation, lymphocytic necrosis increased in number more than that of control chickens. The width of the cortex and medulla decreased. At 24 hours after inoculation, lymphocytic necrosis increased further. At 2 to 5 days after inoculation, the boundary between the cortex and medulla of lobules was obscure and cellular elements of the cortex and medulla were mingled. In experiment II, chickens were necropsied as in experiment I and also at 8 and 14 days after inoculation. The relative weights of the bursa and thymus reduced rapidly to minimal relative weights at 8 days after inoculation. At 14 days after inoculation, both bursa and thymus had normal relative weights and histological structures. These findings indicate that E. coli infection may induce transient lymphocytic depletion of lymphoid tissues in the chicken.


Genetics ◽  
1987 ◽  
Vol 116 (4) ◽  
pp. 513-521
Author(s):  
Nancy J Trun ◽  
Thomas J Silhavy

ABSTRACT The prlC gene of E. coli was originally identified as an allele, prlC1, which suppresses certain signal sequence mutations in the genes for several exported proteins. We have isolated six new alleles of prlC that also confer this phenotype. These mutations can be placed into three classes based on the degree to which they suppress the lamBsignal sequence deletion, lamBs78. Genetic mapping reveals that the physical location of the mutations in prlC correlates with the strength of the suppression, suggesting that different regions of the gene can be altered to yield a suppressor phenotype. We also describe an in vivo cloning procedure using λplacMu9H. The procedure relies on transposition and illegitimate recombination to generate a specialized transducing phage that carries prlC1. This method should be applicable to any gene for which there is a mutant phenotype.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Leonardos Mageiros ◽  
Guillaume Méric ◽  
Sion C. Bayliss ◽  
Johan Pensar ◽  
Ben Pascoe ◽  
...  

AbstractChickens are the most common birds on Earth and colibacillosis is among the most common diseases affecting them. This major threat to animal welfare and safe sustainable food production is difficult to combat because the etiological agent, avian pathogenic Escherichia coli (APEC), emerges from ubiquitous commensal gut bacteria, with no single virulence gene present in all disease-causing isolates. Here, we address the underlying evolutionary mechanisms of extraintestinal spread and systemic infection in poultry. Combining population scale comparative genomics and pangenome-wide association studies, we compare E. coli from commensal carriage and systemic infections. We identify phylogroup-specific and species-wide genetic elements that are enriched in APEC, including pathogenicity-associated variation in 143 genes that have diverse functions, including genes involved in metabolism, lipopolysaccharide synthesis, heat shock response, antimicrobial resistance and toxicity. We find that horizontal gene transfer spreads pathogenicity elements, allowing divergent clones to cause infection. Finally, a Random Forest model prediction of disease status (carriage vs. disease) identifies pathogenic strains in the emergent ST-117 poultry-associated lineage with 73% accuracy, demonstrating the potential for early identification of emergent APEC in healthy flocks.


Sign in / Sign up

Export Citation Format

Share Document