traT Gene Sequences, Serum Resistance and Pathogenicity-related Factors in Clinical Isolates of Escherichia coli and Other Gram-negative Bacteria

Abstract

The R6-5 plasmid-specified outer membrane protein, TraT protein, has previously been shown to mediate resistance to bacterial killing by serum. Colony hybridization with a 700 bp DNA fragment carrying most of the traT gene was used to examine the prevalence of traT in Gramnegative bacteria, particularly strains of Escherichia coli, isolated from clinical specimens. traT was found in isolates of E. coli, Salmonella, Shigella and Klebsiella, but not in Pseudomonas, Aeromonas or Plesiomonas, nor in the few isolates of Enterobacter, Proteus, Acinetobacter, Citrobacter, Serratia or Yersinia that were examined. It was detected in a significantly higher proportion of the E. coli strains isolated from the blood of patients with bacteraemia/septicaemia or from faeces of patients with enteric infections (5670%) than in that of strains isolated from normal faeces (20-40%). The incidence of traT in strains isolated from cases of urinary tract infections was variable. traT was found to be frequently associated with production of the K1 capsule and with the carriage of ColV plasmids, but not with the carriage of R plasmids, nor with serum resistance or the production of haemolysin.

Virulence factors in Escherichia coli urinary tract infection

“…The cloned traT gene increases the serum resistance of unencapsulated strains when present in low copy number, whereas with encapsulated strains, higher copy numbers of traT must be present to affect serum resistance (8). traT is always carried on large IncF plasmids (259,359). Although traT is more common among extraintestinal isolates (58%) than fecal strains (38%) (259), it is not clearly associated in the aggregate with serum resistance (259,359), except possibly among UTI isolates (359), a finding which casts doubt on the importance of traT as a significant determinant of serum resistance in pathogenic strains.…”

“…The best known association of the Kl capsule with human disease is in meningitis, in which 79% of E. coli isolates are positive for the Kl antigen (77,451,473 (42,75,77,359,399,451,473,601).…”

“…Many technical factors influence the results of such assays, including the growth phase of organisms at the time of exposure to serum and the dilution of serum used (dilutions greater than 1/16 have insufficient complement activity to cause killing) (540). Bacterial resistance to killing by serum results from the individual or combined effects of capsular polysaccharide, O-polysaccharide side chains, and surface proteins (359). …”

“…traT. The traT protein is a 25-kDa outer membrane lipoprotein that mediates surface exclusion among strains carrying certain F-like plasmids such as R6-5, R100, and some ColV plasmids (30,358,359,373,540,545). It is a major outer membrane component in these strains (373) and confers a moderate degree of serum resistance by interfering with complement-mediated killing (373,540,545) without affecting complement deposition or inactivating soluble complement (30,359), possibly by inactivating the MAC (359).…”

The TraT Protein is able to Normalize the Phenotype of a Plasmid-carried Permeability Mutation of Salmonella typhimurium

“…This would be the simplest explanation for the results shown here. However, many strains of S. typhimurium or E. coli carry neither plasmids nor traT-like genes (Montenegro et al, 1985), but are nevertheless resistant to hydrophobic agents (Vaara et al, 1985; data on E. coli HBlOl above; unpublished data). In addition, the fact that the introduction of the Salmonella plasmid with the SS-A mutant allele into a plasmidless E. coli strain resulted in increased sensitivity to hydrophobic antibiotics indicates that it is not the lack of the TraT protein but rather the presence of an abnormal SS-A protein that impairs the resistance of the outer membrane.…”