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Escherichia coli bloodstream infections are common and associated with high mortality. A key feature of E. coli is the lipopolysaccharide (LPS) O-antigen, which contributes to immune evasion during invasive infection. We analyzed serial isolates from patients with relapsed E. coli bacteremia and identified frequent disruption of O-antigen synthesis due to mutations in wbbL, resulting in a rough LPS phenotype. Rough LPS isolates were more serum sensitive and less pathogenic in mice. Despite this apparent attenuation, 11 of 61 (18%) E. coli sequence type 131 bloodstream isolates in our cohort harbored disruptive wbbL mutations and were associated with significantly worse clinical outcomes, including septic shock and mortality. Using a murine model of recurrent bacteremia, we show that rough LPS isolates partially evade protective immunity generated against smooth LPS E. coli, highlighting the importance of host immune context in invasive disease.
The degradation of host DNA, and the block to transcription of cytosine-containing DNA, which are a part of the normal course of infection by bacteriophage T4, can be eliminated in an appropriate T4 genetic background (designated as our reference type, or r.t.), so that T4 late promoters carried on plasmid DNA can function. The changes of topoisomer distribution that ensue when phage T4 r.t. infect Escherichia coli carrying a plasmid containing a T4 late promoter were analyzed. The linking number of the covalently closed circular plasmid DNA increased (implying relaxation) at the same time as the distribution of topoisomers became much broader. The relaxation of plasmid DNA was primarily, but not exclusively, due to T4 DNA topoisomerase II. The bacterial DNA topoisomerase II (gyrase) continued to function after phage infection to maintain some degree of superhelicity in plasmid DNA. When the DNA gyrase was inhibited by coumermycin or oxolinic acid, the topoisomer distribution became distinctly bimodal, part of the DNA remaining highly negatively supercoiled. It is argued that the observed post-infection topological changes involve relaxation of torsional stress and changes of binding by proteins that topologically constrain the plasmid DNA.
A technique of continuous filtration of T4-infected Escherichia coli has been devised to study the phenomenon of lysis inhibition. Studies using this technique revealed that the length of the lysis delay caused by superinfection can attain only certain discrete values, which for low average multiplicity of superinfection is thought to be a reflection of the actual number of superinfecting particles per cell. The time interval between primary and superinfection had little effect on the length of lysis delay. With increasing rate of superinfection, the length of lysis delay decreased. In superinfected cells, the concentration of endolysin exceeded the final concentration in nonsuperinfected cells. Superinfection of a lysing culture induced lysis inhibition immediately. Temperature-shift experiments, with cells primarily infected by a temperature-sensitive endolysin mutant, revealed that after the normal latent period superinfection was unable to induce lysis inhibition. Amber-restrictive cells, which were primarily infected by an endolysin negative amber mutant, released adenosine triphosphate (ATP) at the end of the normal latent period although lysis did not occur. Superinfection reduced the loss of ATP markedly. The hypothetical role of the cytoplasmic membrane in lysis inhibition is discussed.
Enteroaggregative Escherichia coli (EAEC) is emerging as a significant diarrheal pathogen in multiple population groups. Although most commonly associated with pediatric diarrhea in developing countries, EAEC is also linked to diarrhea in adults including HIV-positive patients and travelers and has been a cause of food-borne outbreaks in the industrialized world. Current data suggest that one set of virulence elements is not associated with all EAEC strains, but that combinations of multiple factors prevail. Pathogenesis is believed to be initiated with adherence to the terminal ileum and colon in an aggregative, stacked-brick-type pattern by means of one of several different hydrophobic aggregative adherence fimbriae. Some strains of EAEC may then elaborate cytotoxins including the plasmid-encoded toxin and the enterotoxins, EAST1 and ShET1. An AraC homolog termed AggR regulates several genes contributing to fimbrial biogenesis in 'typical EAEC strains'. AggR has now also been shown to regulate genes on a chromosomal island. Sequencing of the EAEC type strain 042 completed at the Sanger Center has revealed two other chromosomal islands that are being explored for their pathogenetic potential. This article reviews these virulence elements and presents on-going areas of research in EAEC pathogenesis.
Infections with non-clostridial gas-forming organisms are not often encountered in orthopaedic practice. We present here a case of gas-forming infection with Escherichia coli which occurred 10 months after internal fixation of a closed fracture of the femur in an 84-year-old diabetic woman who suffered from septic nephrolithiasis. The wound infection was considered to have arisen by spread from the organisms of the infected kidney.
Enteropathogenic Escherichia coli (EPEC) infections are a leading cause of infant diarrhea in developing countries. Recently eaeA, a gene necessary for the characteristic intimate attachment of EPEC to epithelial cells in tissue culture, was described. We conducted a randomized, double-blind study to determine the role of the eaeA gene in human EPEC infection. 11 adult volunteers ingested 2 x 10(10) colony-forming units of O127:H6 EPEC strain E2348/69, and an equal number received the same dose of an isogenic eaeA deletion mutant constructed from E2348/69. Volunteers were monitored for the development of diarrhea, fever, and systemic and gastrointestinal complaints. Diarrhea developed in all 11 volunteers who received E2348/69 and in 4 of 11 who received the mutant (P = 0.002). Fever was more common in recipients of the wild-type strain (P = 0.024). Stool volumes were lower in recipients of the mutant. All volunteers seroconverted to E2348/69 LPS, but the geometric mean peak titers of serum IgG and IgA in recipients of the mutant were lower than those of recipients of the wild-type strain. IgA against LPS was detected in the jejunal fluid of six of six recipients of E2348/69 and 5/6 recipients of the mutant. This study unambiguously assigns a role for eaeA as an EPEC virulence gene, but the residual diarrhea seen in recipients of the mutant indicates that other factors are involved.
Infection of Escherichia coli by bacteriophage T2 was accompanied by a rapid but transient increase in the rate of loss of small molecules from the bacterial cells. This transient leakage was studied with radioactive labels such as (42)K and (28)Mg. Bacteriophage-induced leakage was dependent on the ratio of phage to bacteria: the higher the multiplicity of infection, the greater the leakage. No leakage occurred at 4 C [when adsorption proceeds but injection of phage deoxyribonucleic acid (DNA) is blocked]. Leakage was caused by heavily irradiated phage as well as by normal phage; therefore, the intracellular functioning of the bacteriophage DNA was not required. This conclusion was supported by experiments which showed phage-induced leakage in the presence of chloramphenicol or sodium cyanide. Leakage could be prevented by infecting the bacteria with phage in the presence of high magnesium concentrations. Phage-induced leakage was terminated by a "sealing" reaction, after which potassium turnover by infected and uninfected cells was very similar. The sealing reaction occurred even in the presence of chloramphenicol, suggesting that the sealing is controlled by bacterial and not bacteriophage genes. We were not able to detect any effect of normal bacteriophage infection on the influx (active transport) of potassium and magnesium into the cells.
Escherichia coli O157:H7 differs from previously described diarrheagenic E. coli classes (enteropathogenic, enteroinvasive, enterotoxigenic) by distinct clinical symptoms, production of verotoxin (VT) and a specific plasmid. Cattle are the primary reservoirs of E. coli O157:H7. The organism may be transmitted through the consumption of contaminated foods (mainly of bovine origin) and by person-to-person contact. The most typical clinical manifestations of E. coli O157:H7 infection are hemorrhagic colitis and hemolytic-uremic syndrome. Since the 1982 many outbreaks of E. coli O157:H7 infections as well as sporadic cases have been documented. Diagnosis of E. coli O157:H7 is based on a positive stool culture, presence of VT and elevated serum antibodies. The best currently available and inexpensive method for diagnosing E. coli O157:H7 is culture of stool on sorbitol-Mac Conkey agar medium.
Infections of chickens with Escherichia coli serotype O78 can be treated with the antibiotic sarafloxacin. Three experiments were conducted on the administration of this drug to chickens that had been experimentally infected with E. coli. The birds were monitored for 10 days after infection for their average daily gain (ADG) and feed conversion ratio (FCR), and the post-mortem pathology was assessed. In the first experiment, sarafloxacin (20 mg/L, equivalent to 5 mg/kg live weight per day), given in the drinking water for 3 days after infection, led to a reduction in the mortality from 75% to 27%, but the ADG of the treated birds was still less than that of the uninfected controls. In the second experiment, when the sarafloxacin was administered at the same dose in the water but over only 2 h, there was also a considerable reduction in mortality, and the ADG and the FCR also improved significantly. In the third experiment, the dose dependence of the drug was tested. The birds were given 5 and 10 mg/kg per day sarafloxacin in each group, starting within 2 h after infection. This rapid administration of the drug completely prevented mortality, while the ADG and FCR were similar to those of the uninfected controls.
Enterohemorrhagic Escherichia coli, including the serotype O157:H7 that is most commonly identified with human disease, cause both sporadic cases and outbreaks of non-bloody diarrhea and hemorrhagic colitis. In about 10% of infected subjects, the hemolytic uremic syndrome (hemolytic anemic, thrombocytopenia, and acute renal failure) develops, likely as a consequence of systemic spread of bacterial-derived toxins variously referred to as Shiga-like toxin, Shiga toxin, and Verotoxin. Increasing evidence points to a complex interplay between bacterial products--for example, adhesins and toxins--and host signal transduction pathways in mediating responses to infection. Identification of critical signaling pathways could result in the development of novel strategies for intervention to both prevent and treat this microbial infection in humans.
Enteropathogenic Escherichia coli (EPEC), a leading cause of diarrhea among infants in developing countries, induces dramatic alterations in host cell architecture that depend on a type III secretion system. EspB, one of the proteins secreted and translocated to the host cytoplasm via this system, is required for numerous alterations in host cell structure and function. To determine the role of EspB in virulence, we conducted a randomized, double-blind trial comparing the ability of wild-type EPEC and an isogenic DeltaespB mutant strain to cause diarrhea in adult volunteers. Diarrhea developed in 9 of 10 volunteers who ingested the wild-type strain but in only 1 of 10 volunteers who ingested the DeltaespB mutant strain. Marked destruction of the microvillous brush border adjacent to adherent organisms was observed in a jejunal biopsy from a volunteer who ingested the wild-type strain but not from two volunteers who ingested the DeltaespB mutant strain. Humoral and cell-mediated immune responses to EPEC antigens were stronger among recipients of the wild-type strain. In addition, four of the volunteers who ingested the wild-type strain had lymphoproliferative responses to EspB. These results demonstrate that EspB is a critical virulence determinant of EPEC infections and suggest that EspB contributes to an immune response.