Swine vesicular disease virus. Pathology of the disease and molecular characteristics of the virion

Swine vesicular disease is a highly contagious disease of pigs that is caused by an enterovirus of the family Picornaviridae. The virus is a relatively recent derivative of the human coxsackievirus B5, with which it has high molecular and antigenic homology. The disease is not severe, and affected animals usually show moderate general weakening and slight weight loss that is recovered in few days, as well as vesicular lesions in the mucosa of the mouth and nose and in the interdigital spaces of the feet. However, the similarity of these lesions to those caused by foot-and-mouth disease virus has led to the inclusion of this virus in list A of the Office International des Epizooties. The disease has been eradicated in the European Union except in Italy, where it is considered endemic in the south. Nevertheless, as occasional outbreaks still appear and must be eliminated rapidly, European countries are on the alert and farms are monitored routinely for the presence of the virus. This circumstance has led to a considerable effort to study the pathology of the disease and the molecular biology and antigenicity of the virus, and to the development of optimized methods for the diagnosis of the infection.

Antigenic Homology of the Inducible Ferric Citrate Receptor (FecA) of Coliform Bacteria Isolated from Herds with Naturally Occurring Bovine Intramammary Infections

ABSTRACT Expression of ferric citrate receptor FecA by Escherichia coli and Klebsiella pneumoniae isolated from bovine mastitis was investigated. Transformant E. coliUT5600/pSV66, which produces large quantities of FecA in the presence of citrate, was constructed. The FecA of E. coliUT5600/pSV66 was purified by preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis and used to prepare polyclonal antiserum in rabbits. All coliform isolates of E. coli (n = 18) and K. pneumoniae(n = 17) from naturally occurring bovine intramammary infections in five herds induced iron-regulated outer membrane proteins when grown in Trypticase soy broth containing 200 μM α-α′-dipyridyl and 1 mM citrate. Polyclonal antiserum against FecA was used in conjunction with an immunoblot technique to determine the degree of antigenic homology of FecA among isolates. In the presence of citrate, each isolate expressed FecA that reacted with the anti-FecA polyclonal antiserum. The molecular mass of FecA (∼80.5 kDa) was also highly conserved among isolates. Therefore, the ferric citrate iron transport may be induced in coliform bacteria and utilized to acquire iron in milk for survival and growth. The FecA is an attractive vaccine component for controlling coliform mastitis during the lactation period.

Serological Discrimination of Dogs Infected with Gastric Helicobacter spp. and Uninfected Dogs

Characterization of the humoral immune responses of people toHelicobacter pylori infection has facilitated the investigation of the host response to bacterial virulence factors and the development of sensitive and specific diagnostic tests. Dogs are commonly infected with gastric Helicobacter spp., but the presence of multiple Helicobacter spp. and possible coinfection in individual dogs have complicated serological evaluation. Evaluation of the antigenic homology of Helicobacter spp. revealed that the major protein bands of Helicobacter felisand Helicobacter bizzozeronii, two Helicobacterspp. that infect dogs, were very similar to UreA (29 to 31 kDa), UreB (63 to 66 kDa), and HSP (58 to 60 kDa) of H. pylori, and sera from infected and uninfected dogs bound in a similar way to each antigen. Immunoblotting and an enzyme-linked immunosorbent assay (ELISA) with H. felis ATCC 49179 antigen were performed with 101 serum samples (from 78 infected dogs and 23 uninfected dogs). Samples from uninfected dogs (median = 8) had fewer bands on immunoblotting than samples from infected dogs (median = 16) (P < 0.05). Combinations of the presence of any two of the low-molecular-mass bands (19, 25, 30, 32, and 37 kDa) or the high-molecular-mass bands (86 and 94 kDa) were found almost solely in samples from infected dogs (P < 0.0001). Kinetic ELISA results were significantly higher for samples from infected dogs (median = 0.0802 optical density unit [OD]/min) than for samples from uninfected dogs (median = 0.01428 OD/min). The combination of ELISA and immunoblotting results gave a specificity of 95.6% and a sensitivity of 79.8%. No correlation between ELISA results, colonization density, degree of inflammation, and presence of lymphoid follicles was observed. The results indicate substantial antigenic homology between H. felis, H. pylori, andH. bizzozeronii. The combination of ELISA and immunoblotting was a highly specific and moderately sensitive indicator of infection. The degree of seropositivity assessed by ELISA was not related to bacterial colonization density, the degree of gastric inflammation, or the presence of lymphoid follicles.

RHIZOBIUM COMPETITION IN ANTIGUAN SOILS: STRAIN ISOLATION

The enzyme-linked immunosorbent assay was used to determine the competitive ability of three Rhizobium strains introduced into Antiguan soil. Strain-specific antisera were prepared against each strain. Field experiments were conducted in Antigua using Rhizobium strains USDA 3384, USDA 3473, and USDA 3474 as a peat-base inoculant and pigeon pea as the test crop. Nodules from the respective treatments were removed and prepared for ELISA studies. There was cross reactivity between the antisera, but it was greatly reduced or eliminated by repeat adsorption with the cells of the cross-reacting strains. Nodule occupancy by plants treated with Rhizobium 3384, 3473, and 3384 was 70%, 90%, and 100%, respectively. Nodules from 3384 and 3474 treated plants contained cells with no antigenic homology to the three antisera. We concluded that these nodules were developed from indigenous Rhizobium strains found in Antiguan soils.