The temperature-sensitive hemagglutinin Tsh is a member of the autotransporter group of proteins and was first identified in avian-pathogenic Escherichia coli (APEC) strain 7122. The prevalence of tsh was investigated in 300 E. coli isolates of avian origin and characterized for virulence in a 1-day-old chick lethality test. Results indicate that among the tsh-positive APEC isolates, 90.6% belonged to the highest virulence class. Experimental inoculation of chickens with 7122 and an isogenic tsh mutant demonstrated that Tsh may contribute to the development of lesions within the air sacs of birds but is not required for subsequent generalized infection manifesting as perihepatitis, pericarditis, and septicemia. Conjugation and hybridization experiments revealed that the tsh gene is located on a ColV-type plasmid in many of the APEC strains studied, including strain 7122, near the colicin V genes in most of these strains. DNA sequences flanking the tsh gene of strain 7122 include complete and partial insertion sequences and phage-related DNA sequences, some of which were also found on virulence plasmids and pathogenicity islands present in various E. coli pathotypes and other pathogenic members of the Enterobacteriaceae. These results demonstrate that the tsh gene is frequently located on the ColV virulence plasmid in APEC and suggest a possible role of Tsh in the pathogenicity of E. coli for chickens in the early stages of infection.Avian-pathogenic Escherichia coli (APEC) comprise a specific subset of pathogenic E. coli that cause extraintestinal diseases of poultry. Of the various forms of E. coli disease in poultry, the most common syndrome starts as a respiratory tract infection in 3-to 12-week-old broiler chickens and turkeys and frequently becomes more generalized. The air sacs are the first organs affected, and systemic spreading may result in pericarditis, perihepatitis, and an often fatal septicemia (15,29). APEC infections are frequently enhanced or initiated by predisposing factors, which include environmental conditions and viral or Mycoplasma infection (15, 29). O1, O2, and O78 are the most commonly encountered serogroups among APEC (15,29), and the majority of strains have been shown to belong to a limited number of clonal lineages (69, 70). APEC strains of high virulence are lethal for 1-day-old chicks when administered subcutaneously. Attributes associated with APEC strains include F1 (type 1) and P fimbrial adhesins (16, 21, 53, 66), resistance to serum and phagocytosis (21, 22, 52, 71), the aerobactin siderophore system (21, 41, 65), and colicin V (7, 23, 65, 71) (reviewed in references 15 and 29). Recently the tsh gene, encoding a temperature-sensitive hemagglutinin, first identified by Provence and Curtiss (54), was shown to be associated with APEC but not with E. coli isolated from the feces of healthy chickens (45).The tsh gene was first identified from APEC O78:K80 strain 7122 and, when cloned into E. coli K-12, was shown to impart mannose-resistant hemagglutination of chicken erythrocytes...

In chickens, colibacillosis is caused by avian pathogenic Escherichia coli (APEC) via respiratory tract infection. Many virulence factors, including type 1 (F1A) and P (F11) fimbriae, curli, aerobactin, K1 capsule, and temperature-sensitive hemagglutinin (Tsh) and plasmid DNA regions have been associated with APEC. A strong correlation between serum resistance and virulence has been demonstrated, but roles of virulence factors in serum resistance have not been well elucidated. By using mutants of APEC strains TK3, MT78, and 7122, which belong to serogroups O1, O2, and O78, respectively, we investigated the role of virulence factors in resistance to serum and pathogenicity in chickens. Our results showed that serum resistance is one of the pathogenicity mechanisms of APEC strains. Virulence factors that increased bacterial resistance to serum and colonization of internal organs of infected chickens were O78 lipopolysaccharide of E. coli 7122 and the K1 capsule of E. coli MT78. In contrast, curli, type 1, and P fimbriae did not appear to contribute to serum resistance. We also showed that the iss gene, which was previously demonstrated to increase resistance to serum in certain E. coli strains, is located on plasmid pAPEC-1 of E. coli 7122 but does not play a major role in resistance to serum for strain 7122.Avian pathogenic Escherichia coli (APEC) belongs to the extraintestinal pathogenic group of E. coli. These bacteria cause airsacculitis, omphalitis, peritonitis, salpingitis, synovitis, and colisepticemia in poultry (17). APEC is also associated with cellulitis or necrotic dermatitis of the lower abdomen and thighs and with granuloma. APEC strains belong predominantly to three serogroups, O1, O2, and O78. Virulence factors associated with APEC strains include type 1 and P fimbriae, curli, aerobactin, K1 capsule, and temperature-sensitive hemagglutinin (Tsh) of the autotransporter family (9, 17). Serum resistance also appears to be an important virulence mechanism of APEC, and it may play a major role in the pathogenesis of avian colibacillosis. For instance, serum resistance has often been associated with isolates from septicemic turkeys and chickens (13,33), and a correlation between serum resistance and virulence and lethality in isolates from septicemic chickens and turkeys has been observed (13,15,17).At this time, it is not known if avian E. coli strains differ from mammalian isolates in their mechanisms of serum resistance and virulence. Studies carried out with mammalian E. coli showed that many virulence factors, such as capsules, lipopolysaccharide (LPS), and outer membrane proteins (OMPs), includingOmpA and the ColV plasmid-encoded proteins TraT and Iss, are associated with complement resistance of E. coli (17). TraT is a surface exclusion protein encoded by conjugative plasmids (32), and Iss is a plasmid-encoded OMP homologous to the Bor protein of bacteriophage (32). In APEC, the role of different virulence factors in serum resistance has generally been speculative. Nolan et al. (22) produced an a...

Fumonisin B 1 (FB 1 ) is a mycotoxin that commonly occurs in maize. FB 1 causes a variety of toxic effects in different animal species and has been implicated as a contributing factor of esophageal cancers in humans. In the present study, we examined the effect of dietary exposure to FB 1 on intestinal colonization by pathogenic Escherichia coli associated with extraintestinal infection. Three-week-old weaned pigs were given FB 1 by gavage as a crude extract or as a purified toxin at a dose of 0.5 mg/kg of body weight daily for 6 days. On the last day of the toxin treatment, the pigs were orally inoculated with an extraintestinal pathogenic E. coli strain. All animals were euthanized 24 h later, necropsies were performed, and tissues were taken for bacterial counts and light microscopic examination. Ingestion of FB 1 had only a minimal effect on animal weight gain, did not cause any macroscopic or microscopic lesions, and did not change the plasma biochemical profile. However, colonization of the small and large intestines by an extraintestinal pathogenic E. coli strain was significantly increased. Our results show that FB 1 is a predisposing factor to infectious disease and that the pig can be used as a model for the study of the consequences of ingesting mycotoxin-contaminated food.

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Escherichia coli 045 isolates associated with swine postweaning diarrhea in Quebec were characterized with respect to virulence determinants genetically and investigated for their attaching and effacing (A/E) activities by experimental inoculation of gnotobiotic piglets and by the HEp-2 cell adherence assay. All of 32 isolates tested were negative for enterotoxigenic and verotoxigenic E. coli virulence determinants, heat-labile enterotoxin (LT), heat-stable enterotoxins (STap, STb), verotoxins (VT1, VT2), and F4 (K88), F5 (K99), F6 (987P), and F41, except one STh-positive and two F4-positive isolates. A total of 25 isolates hybridized with an EaeA probe, and 11 hybridized with an enteropathogenic E. coli adherence factor (EAF) probe. None of 32 isolates hybridized with a bundle-forming pilus (BFP) probe. The EAF, EaeA, and BFP factors have been associatedwith human enteropathogenic E. coli strains. A total of 10 of 12 eaeA-positive porcine 045 isolates induced A/E lesions characterized by intimate adherence of bacteria to the intestinal epithelial cell membrane with effacement of the microvilli, similar to those of human attaching-effacing E. coli. However, A/E lesions were not observed in the piglets inoculated with any one of three eaeA-negative 045 isolates. All E. coli 045 isolates were non-adherent to HEp-2 cells. Thus, we have demonstrated the production of typical A/E lesions by nonenterotoxigenic E. coli 045 isolates from swine postweaning diarrhea. The results indicate the significance of the eaeA gene in A/E activities of these isolates and suggest that EAF and BFP are not involved in 045 E. coli infection of weaning piglets.