We have cloned the replicative form (RF-) DNA of mink enteritis virus (MEV), constructed an infectious recombinant plasmid containing MEV DNA and determined the nucleotide sequence of the clbned MEV DNA. RF-DNAs were detected and infectious virus was generated when the recombinant plasmid containing the entire MEV genome was introduced into feline kidney cell cultures. The MEV genome was 5094 nucleotides (nt) in length; the 3' end of the virion strand contained a 205 nt palindromic sequence and the 5' end a 62 nt palindromic sequence that could assume Y-and U-shaped configurations, respectively. The 5' end of the virion strand had a direct repeat of 61 nt at the carboxyl terminus of the capsid protein gene. The organization of the MEV genome is similar to those of canine parvovirus (CPV) and feline panleukopenia virus (FPLV); there are two large open reading frames (ORFs), one in the 3' half and the other in the 5' half of the genome, with coding capacities of 668 and 722 amino acid residues, respectively. Both are in the same reading frame and no significant ORFs are apparent in the virion strand (negative-sense strand). Possible functional promoter motifs are located at map unit (m.u.) 4-5 and m.u. 40, and a possible functional poly(A) signal is located at m.u. 96. The nucleotide and amino acid sequence homology with CPV and FPLV is greater than 98 %, consistent with the hypothesis that MEV and CPV are host-range variants of FPLV.

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A genotypic comparison using pulsed‐fleld gel electrophoresis (PFGE), amplified ribosomal restriction analysis (ARDRA) as well as PCRs targeting virulence associated genes reported elsewhere in avian pathogenic Escherichia coli (APEC) was made between E. coli strains isolated from chickens with colibacillosis and those from the feces of apparently healthy chickens in Japan. The majority (67%) of clinical isolates belonged to a certain phylogenetic ARDRA but not PFGE cluster, with virulence‐related genes carried by ColV plasmid being markedly prevalent. The result suggests that APEC strains originated from the same “ancestor” in the course of E. coli evolution.

One hundred and twenty 30-day-old specific-pathogen-free chickens were inoculated with the liposomal inactivated avian pathogenic Escherichia coli (APEC) vaccine by eye drop or coarse spraying. All of the chickens produced anti-lipopolysaccharide antibodies of the IgG subclass in their sera as well as IgA antibodies in their oral mucus. The results demonstrated a rise in antibodies in the serum of chickens administered the APEC vaccine through nonparenteral mucosal routes. Bacterial counts in the blood decreased, and clinical signs were moderated in the vaccinated chickens after challenge with a strain of APEC. No harmful effects from the vaccination were observed. The liposomal inactivated APEC vaccine described in this paper would contribute to a practical method of control for avian colibacillosis.

In iron-limiting environments, Salmonella enterica serovar Enteritidis and Salmonella enterica serovar Typhimurium synthesize and secrete several types of siderophore to trap trivalent ferric ions; these bacteria then express siderophore receptors called iron-regulated outer membrane proteins (IROMPs). In this study, we experimentally reproduced iron-limiting environments using a divalent metal chelator. IroN, one of the IROMPs, was purified by affinity chromatography with an anti-IroN-MAb-immobilized column. Thirty-day-old chickens were immunized intramuscularly with purified IroN from Salmonella Typhimurium mixed with Freund's incomplete adjuvant; the chickens were then challenged intravenously with Salmonella Enteritidis. The mortality rate of immunized chickens was 10%. On the other hand, that of control chickens was 80%. By Western blot analysis, specific IgG antibody responses against IroN of Salmonella Enteritidis were identified in chickens immunized with purified IroN. These results indicate that IroN might be promising as an important vaccine component against Salmonella infection in chickens.