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The concentration of the amyloid AA-related serum protein (SAA) was markedly increased after endotoxin injections in mink, mouse, rabbit, and man. It was particularly studied during the development of endotoxin-induced amyloidosis of the mink. Protein SAA was markedly elevated in all mink 24 h after the first endotoxin injection but had fallen to relatively low levels before the onset of amyloidosis at about 4 wk. These results are consistent with SAA being a circulating precursor of the amyloid fibril protein, AA. However, both proteins may be derived by proteolysis from a common precursor.

The serum proteins in 1 group of healthy breeders, 1 group of healthy pups and 4 groups of foxes suffering from various diseases were separated electrophoretically on cellulose acetate membranes. In most of the sera, the proteins were separated into 1 albumin fraction and 5 globulin fractions designated alpha1, alpha2, alpha3, beta and gamma. The mean concentrations of the total proteins and the various serum fractions in the disease groups were compared statistically with the mean values of the normal groups.

The serum proteins in Sapphire mink from the experimental and control groups in 2 endotoxin experiments and in a group of normal mink of the Standard type, were separated electrophoretically on cellulose acetate membranes.

An outbreak of endometritis and septicaemia in farms that raise Arctic blue foxes is described. Eleven animals from eight different farms were examined, most of them pregnant or with newly delivered litters. Pathological examination indicated inflammation of the uterus, and focal necrotic changes in the liver. In some animals evidence of hemorrhaging was found in the anterior part of the small intestine. Bacteriological examination revealed abundant growth from different organs of the animals of a pure culture of a small, slender, Gram-variable, sporeforming rod, which was identified phenotypically as aerotolerant Clostridium carnis. This identification was confirmed by DNA hybridization. The organism caused death in mice 1–2 days after intraperitoneal inoculation, and killed an Arctic blue fox which was inoculated intracervically. Two foxes, pretreated with diethyl-stilboestrol, became seriously ill after intrauterine inoculation, but survived. The spontaneous outbreak of the disease was characterized by sudden onset of septicaemia with few or no clinical symptoms before the animals succumbed.

Post-traumatic lung insufficiency in dogs was induced by a combination of haemorrhagic hypotension and liver trauma. In one experimental group, lung biopsies were sampled every 4 h. This paper describes the development of gross and light microscopic lunig changes in these dogs, and the lung lesions 12 h after initiation of the trauma in another experimental group. Incipient changes were recognized as early as 4 h after initiation of the trauma. Perivascular and intraseptal oedema, scattered microthrombi, and trapping of leucocytes in lung microvessels were the most conspicuous morphological findings. These changes grew gradually more pronounced towards collapse, when also areas with interstitial haemorrhages, intra-alveolar protein-rich oedema fluid with strands of a fibrinoid material, and an increased number of partly degenerated leucocytes were found in addition to atelectasis.

Four pigs were injected intravenously twice at a 24-hour interval with disintegrated cells of Haemophilus parainfluenzae and killed 24 h later. Two of the pigs developed bilateral renal cortical necrosis (BCN) and renal and extrarenal vascular lesions characterized by fibrinous thrombosis and fibrinoid degeneration. The BCN is interpreted as being the result of a generalized Shwartzman reaction to bacterial endotoxin. The experiment supports the view that the vascular lesions accompanying outbreaks of Haemophilus infections in swine are due to a generalized Shwartzman reaction.

Six cases representing three species, previously diagnosed as bilateral renal cortical necrosis (BCN), were studied histologically. One horse had vascular lesions including fibrinoid necrosis and fibrinous thrombi in various organs. Intrarenally these lesions occurred in interlobular arteries, afferent arterioles, and glomeruli. Another horse had bilateral renal glomerular thrombosis but no extra-glomerular vascular lesion. Distinct fibrinous deposition in the renal vessels did not occur among the other four cases. A comparison is drawn between the characteristic lesions in the generalized Shwartzman reaction (GSR) and BCN as diagnosed in our autopsy material. The renal alterations were compatible with GSR in two horses only among the six cases.