The pathogenesis of haemorrhagic septicaemia in buffalo infected with Paste
urella multocida is poorly understood. However, the characteristic of sudde
n onset leading to the rapid death of infected animals is similar to that s
een in other clinical conditions known to involve endotoxic shock. The obje
ctives of the work were to assess the contribution of endotoxaemia to the d
isease's pathogenesis and to characterize the pathophysiological reaction,
including the acute phase response, of buffalo to experimental infection wi
th P. multocida serotype B:2, the bacterium responsible for the disease in
Asia. After intranasal infection of eight buffaloes with a culture of a fie
ld isolate of P. multocida serotype B:2, three animals succumbed to the dis
ease at 26-30 h post-infection (p.i.) and five survived. Rectal temperature
s of infected animals rose to a peak at about 10 h p.i. and surviving anima
ls showed a second peak in rectal temperature at 36 h p.i. Endotoxin was pr
esent only in serum of non-surviving animals 3-5 h before death or killing
during which time concentrations increased rapidly, correlating with the de
velopment of overt clinical signs and reductions in rectal temperature, con
centrations of white blood cells, serum thyroxine, iron, copper and zinc, a
n increase in serum haptoglobin and cortisol and the detection of a low-gra
de bacteraemia. A strong acute phase response was maintained in surviving a
nimals with a progressive rise in serum haptoglobin over 96 h p.i., a slow
rise in the serum copper concentration from 24 h p.i. and an increase, from
about 65 h p.i., in serum alpha (1)-acid glycoprotein. The findings demons
trate that a progressive endotoxaemia and associated sequelae correlates wi
th the development of overt haemorrhagic septicaemia disease and sudden dea
th in buffalo. (C) 2001 Academic Press.