scholarly journals The Generalized Shwartzman Reaction and Haemophilus Infections in Pigs

1967 ◽  
Vol 4 (3) ◽  
pp. 245-253 ◽  
Author(s):  
K. Nordstoga ◽  
M. Fj⊘lstad

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.

1967 ◽  
Vol 4 (3) ◽  
pp. 233-244 ◽  
Author(s):  
K. Nordstoga

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.


1964 ◽  
Vol 12 (02) ◽  
pp. 462-470 ◽  
Author(s):  
F Rodríguez-Erdmann

SummaryAnimals treated in the conventional form to elicit the generalized Shwartzman reaction (gSr) by means of properly spaced injections of endotoxin develop an abrupt consumption of the plasmatic factors of the clotting mechanism, as demonstrated by the reduction of the activity of prothrombin and Ac-G (factor V). These animals show ultimatly characteristic morphological pattern: bilateral cortical necrosis of the kidney. Rabbits treated four hours after the second (‘‘provocative”) endotoxin injection with streptokinase (Varidase/Lederle) in order to activate the fibrinolytic system failed to develop the renal cortical necrosis, but their prothrombin and Ac-G (factor V) level decreased abruptly.Through indirect deduction the intravascular presence of thrombin-like activity is accepted four hours after the “provocative” endotoxin injection.


1958 ◽  
Vol 107 (3) ◽  
pp. 377-381 ◽  
Author(s):  
Sandor S. Shapiro ◽  
Donald G. McKay

Using intravenous sodium warfarin, rabbits were rendered hypoprothrombinemic and subjected to two intravenous injections of Shear's polysaccharide. None of the 9 animals surviving the required period of time developed bilateral renal cortical necrosis or histologic thrombi in the kidney, liver, spleen, or lungs. In a control group of 7 animals treated only with endotoxin, 6 developed bilateral renal cortical necrosis. It is concluded that the prothrombin complex is necessary for the production of the generalized Shwartzman reaction by bacterial endotoxins and that this phenomenon is essentially a process of disseminated intravascular coagulation.


1967 ◽  
Vol 18 (01/02) ◽  
pp. 024-039 ◽  
Author(s):  
S. A Evensen ◽  
M Jeremic ◽  
P. F Hjort

SummaryLiquoid (sodium polyanethol sulfonate), a synthetic heparin-like anticoagulant, produces renal cortical necrosis in rabbits. This lesion is indistinguishable from the generalized Shwartzman reaction which is caused by intravascular coagulation in a prepared animal. We have investigated this apparently paradoxic effect of Liquoid. Our main findings are:1. Liquoid is a potent heparin-like anticoagulant. One mg of Liquoid is neutralized by 1 mg of Polybrene. After intravenous injection the anticoagulant effect is immediate and persists for several hours.2. In larger concentrations, Liquoid precipitates fibrinogen. The precipitation does not depend on an intact coagulation system; the precipitates are dissolved in 30% urea.3. An intravenous injection of 20 mg Liquoid/1500 g body-weight produces an early thrombocytopenia, a progressive depletion of fibrinogen and factor V, the appearance of cold-precipitating material in plasma, and severe renal cortical necrosis.4. Pretreatment with warfarin completely prevents all of these effects, except a moderate fall in platelets.We conclude that Liquoid produces these effects, not by precipitation of fibrinogen, but by intravascular coagulation, probably released through aggregation and damage of the platelets. Thus, intravascular coagulation is again confirmed as the final event in the generalized Shwartzman reaction.


1963 ◽  
Vol 117 (3) ◽  
pp. 365-376 ◽  
Author(s):  
Leung Lee

In the presence of reticuloendothelial blockade, the intravenous injection of a protein antigen into specifically immunized rabbits or the infusion of soluble immune complexes into normal animals has been shown to result in the production of bilateral renal cortical necrosis. The similarity in the pathogenesis of this lesion and that seen in the classical generalized Shwartzman reaction produced by bacterial endotoxins is indicated by (a) the failure of both lesions to develop in animals pretreated with large doses of heparin, (b) by the finding of "heparin-precipitable fibrinogen" in the circulation, and (c) by the presence of massive fibrin deposits within the glomerular capillaries. These findings indicate that antigen-antibody reactions in vivo are capable of activating the blood coagulation system and that the mode of action of bacterial endotoxins may have an immunological basis.


1969 ◽  
Vol 16 (5) ◽  
pp. 507-516 ◽  
Author(s):  
Edwin N. Forman ◽  
Charles F. Abildgaard ◽  
Jane F. Bolger ◽  
Christine A. Johnson ◽  
Irving Schulman

1970 ◽  
Vol 24 (01/02) ◽  
pp. 136-145 ◽  
Author(s):  
J. J Corrigan

SummaryRabbits given 2 properly spaced intravenous injections of bacterial endotoxin develop bilateral renal cortical necrosis (generalized Shwartzman reaction - gSr). This renal lesion is the result of fibrin deposition secondary to diffuse intravascular clotting (DIC). Using this experimental model, the effect of anticoagulating (large) and non- anticoagulating (small) concentrations of heparin on the changes in blood platelets, plasma coagulation factors II, V, VIII and fibrinogen during the production of renal cortical necrosis was studied. The data demonstrate that all amounts of heparin given during, but not after, the period of intravascular clotting reduced the frequency of renal cortical necrosis. Anticoagulating concentrations completely prevented the renal lesion. Non-anticoagulating amounts could reduce the frequency of the renal lesions, but this effect was not predictable or consistent. Coagulation studies in the large dose group revealed thrombocytopenia reduced factors II, V, and VIII but no fibrinogen consumption. These findings suggest that heparin inhibits the formation of fibrin in vivo, thereby preventing the formation of renal cortical necrosis. The coagulation data in the small dose group differed in that fibrinogen consumption did occur. The possible explanations for the phenomenon were discussed.


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