The potential role of the Arthus and Shwartzman reactions in the pathogenesis of pneumonic pasteurellosis.

Pneumonic pasteurellosis (PP) is an economically important disease in cattle, sheep, and goats. Pasteurella haemolytica is commonly isolated from the severe fibrinopurulent pneumonia that characterize this respiratory syndrome. During infection, the bacteria produce leukotoxin (LKT) and lipopolysaccharide (LPS), both potent inducers of inflammation. Nonetheless, it has also been demonstrated that an exacerbated host's inflammatory response is responsible for the severe lung damage. Despite research in this field, the pathogenesis of PP is still incomplete. Two classical models of acute inflammatory response induced in laboratory animals, the Arthus and Shwartzman reactions, could explain the pathogenesis of the severe lung lesions that characterize PP.

Lesions resulting from attempted Shwartzman reaction in turkey poults inoculated with Pasteurella multocida lipopolysaccharide.

Five-week-old turkey poults were given two consecutive intravenous injections (24 hours apart) of highly purified Pasteurella multocida lipopolysaccharide (LPS) in an effort to induce a generalized Shwartzman reaction. There were no gross lesions, and microscopic lesions were limited to focal hepatic necrosis with heterophil infiltration. Hepatic lesions did not differ qualitatively from lesions in turkeys given a single dose of lipopolysaccharide. Margination of heterophils in the pulmonary vasculature was observed in turkeys 4 hours after a single injection of LPS, but it was not present in turkeys given the consecutive injections of LPS. To induce a dermal Shwartzman reaction, turkeys were given intradermal injections of LPS followed by an intravenous injection of LPS 24 hours later. Although no grossly visible hemorrhagic dermal necrosis occurred, microscopic lesions, including heterophil infiltration, vasculitis, thrombosis, and necrosis, were present. Thrombosis and vasculitis were observed only in turkeys given the intravenous and intradermal LPS, whereas the other inflammatory changes were observed in turkeys given the intradermal injection of LPS and intravenous water. Prominent lymphocytic perivascular cuffing at the site of dermal injection was present in all turkeys given intradermal LPS.

Attempted induction of local Shwartzman reaction in the chicken.

Chickens and rabbits were injected intradermally with an endotoxin, namely Escherichia coli lipopolysaccharide (LPS). Twenty-four hours later, LPS was again administered intravenously to induce a local Shwartzman reaction. A typical cutaneous inflammatory reaction developed in rabbits, but not in chickens. Even very high doses of LPS, that made the birds visibly sick, failed to elicit the reaction. The results suggest that chickens are refractory to the Shwartzman reaction. A noteworthy feature of the chickens' response to intradermal endotoxin was the formation of prominent perivascular lymphoid aggregates.

Effects of Pasteurella multocida endotoxins on turkey poults.

Studies of turkey poult responses to Pasteurella multocida endotoxins indicated that lipopolysaccharide (LPS) preparations from two highly pathogenic strains and free endotoxin from one of these strains were all similar in lethal toxicity. Lethal intravenous doses were generally high, 1 mg or more for 1-week-old poults (13.3 mg/kg). The toxic effects of LPS were not increased by repeated administration of small hourly doses. For both forms of endotoxin, the relationship between dose and response was considered erratic. Attempts to increase the susceptibility of poults to LPS by administering a liver-damaging substance (galactosamine) or a histamine-releasing substance (compound 48/80) or by performing surgical bursectomy were not effective. The LPS did not provoke a dermal Shwartzman reaction, even though doses used were 10 times those that produced a characteristic reaction in a rabbit.