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ARS Home » Research » Publications at this Location » Publication #83484
Title: CONTRIBUCION MAYOR DEL INOCULO POR VIA RESPIRATORIA EN EL DESARROLLO DE LA REACCION DE SHWARTZMAN EN EL PULMON DEL CONEJO

Author
item RAMIREZ-ROMERO, R - UANL, MEXICO
item Brogden, Kim
item Cutlip, Randall

Submitted to: Veterinaria Mexico
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/18/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Respiratory tract diseases are a leading cause of loss from disease in the cattle, sheep and goat industries. Annual loss in the United States is estimated to exceed one billion dollars. Losses are from mortality, reduced feed efficiency, and slaughter condemnations, as well as prevention and treatment measures. Currently, not all the factors leading to the development of pneumonia are known by scientists and veterinarians. As part of our ongoing studies to understand the disease process, we found that bacterial extracts can lead to inflammation of the lungs of rabbits. This inflammation was similar to that seen on naturally occurring cases of the disease. On the basis of our findings, it appears that this would be an important factor in the disease process. Our findings are an important first step in the development of a new vaccine that can be used to better control shipping fever of cattle. Corollary benefits include an increase in the profitability and international competitiveness of the U. S. cattle industry, a stronger rural economy, and a continued supply of inexpensive, wholesome beef, and beef products for the American consumer.

Technical Abstract: The Shwartzman reaction (SR) can be induced in the lungs of rabbits with Pasteurella haemolytica lipopolysaccharide (LPS) and resembles, at least in part, the lesions seen in natural cases of bovine pneumonic pasteurellosis. To demonstrate this, 2 groups of rabbits were inoculated with LPS. Rabbits in group 1 received an intratracheal (IT) inoculation of LPS (100 ug). Rabbits in group 2 received an IT inoculation of LPS (100 ug) and a second intravenous (IV) inoculation of LPS (100 ug). At 36 h post IT injection of LPS, all rabbits were killed. The lungs were excised and saline (15 ml) was infused in and out of the left side of the lung to remove macrophages and infiltrated cells. Total and differential cell counts were done. There was no difference in the total cell number recovered between groups (P > 0.05). However, the number of macrophages were higher in Group 2 (P < 0.05) and the number of neutrophils were higher in Group 1 (P < 0.05). These results suggest that LPS plays a role in the pulmonary inflammatory response provoked by the SR.