Pulmonary lesions in mice inoculated with Actinobacillus pleuropneumoniae hemolysin and lipopolysaccharide.

Non-Swiss albino (CF1) male mice were used as a model to study the effects of specific toxic components of Actinobacillus pleuropneumoniae on the respiratory system. Mice were divided into five groups of ten each and were inoculated by the intranasal route with whole-cell Actinobacillus pleuropneumoniae serotype 1, cell-free culture supernatant fluid (CFCSF) containing hemolysin protein, purified lipopolysaccharide (LPS), heat-treated CFCSF, or phosphate-buffered saline solution. Pulmonary lesions were evaluated at 6 and 12 hours after inoculation.

Inhibition of bactericidal activity of anticapsular antibody by nonspecific antibodies reactive with surface-exposed antigenic determinants on Actinobacillus pleuropneumoniae.

In an attempt to understand the mechanism of serum resistance in Actinobacillus pleuropneumoniae, in the present study we examined various interactions among the bacterial surface constituents, serum antibodies, and complement. Analysis of swine sera revealed the presence of anticapsular antibodies in convalescent-phase sera but not in preimmune sera. Both types of sera contained antibodies which reacted with each of 14 polypeptides present in saline extracts of the bacteria.

Effects of Actinobacillus pleuropneumoniae hemolysin on porcine neutrophil function.

In an attempt to gain insight into the events that take place during Actinobacillus pleuropneumoniae infection, the present study was designed to ascertain the effects of bacterial toxicity on porcine neutrophil functions and viability. Incubation of phagocytes (2 x 10(6)) with opsonized A. pleuropneumoniae 4074 (2 x 10(7) CFU) resulted in phagocytic uptake of less than or equal to 4%.

Role of haemophilus pleuropneumoniae lipopolysaccharide endotoxin in the pathogenesis of porcine Haemophilus pleuropneumonia.

Intact Haemophilus pleuropneumoniae cells (strain Shope 1, serotype 1), highly purified lipopolysaccharide (LPS) obtained from this strain of H pleuropneumoniae, as well as from Escherichia coli O111:B4, filter-sterilized H pleuropneumoniae cell-free culture supernatant fluid, and heat-inactivated supernatant fluid were given intranasally to CF1 mice and intratracheally to pigs. Pulmonary lesions induced by H pleuropneumoniae in mice were similar to those induced by H pleuropneumoniae in pigs. Histologically, lungs of mice and pigs killed 1 or 2 days after inoculation with 200 micrograms of highly purified H pleuropneumoniae LPS had lesions similar to one another and were similar to those in mice and pigs given intact H pleuropneumoniae, except that little or no necrosis or hemorrhage was observed.

Relationship of iron administration to susceptibility of newborn pigs to enterotoxic colibacillosis.

To determine whether supplemental iron (Fe) administration to newborn pigs reared in concrete pens not only prevents anemia, but renders the pigs more susceptible to Escherichia coli-induced diarrheal disease, pigs were given a large or a small dose of Fe IM or orally before or after challenge exposure with E coli. The controls were challenge-exposed pigs not given Fe and pigs not challenge exposed (Fe-treated and nontreated groups). Although the mortality of the pigs challenge exposed with E coli and administered a large oral dose of Fe shortly after birth was greater than that of the challenge-exposed pigs given no Fe, differences in mortality were not noted between any of the groups tested when the Fe was injected IM.