scholarly journals THE DEVELOPMENT OF THE ACUTE INFLAMMATORY RESPONSE TO EXPERIMENTAL CUTANEOUS MUCORMYCOSIS IN NORMAL AND DIABETIC RABBITS

1959 ◽  
Vol 110 (6) ◽  
pp. 845-852 ◽  
Author(s):  
Walter H. Sheldon ◽  
Heinz Bauer

The histologic changes associated with the development of the acute inflammatory response to experimental cutaneous mucormycosis were studied at various times from 5 minutes to 24 hours after inoculation into normal rabbits and in rabbits with acute alloxan diabetes and acidosis. In normal animals the response by polymorphonuclear leukocytes began within a few minutes after inoculation, increased rapidly in extent and intensity and reached its peak within 6 to 12 hours. By that time there was also early proliferation of fibroblasts and of large mononuclear cells and these cellular reactions, together with the accumulated granulocytes, began to produce a demarcation of the lesions. Beginning 4 to 6 hours after inoculation the fungus showed some growth but this remained confined to the necrotic center of the lesions. In the diabetic rabbits the onset of the response by polymorphonuclear leukocytes was delayed by several hours, reduced in intensity and was apparently less effective. There was no proliferation of fibroblasts and the lesions were spreading rather than circumscribed. Fungus growth in the tissues began shortly after inoculation, was marked, progressed rapidly, and soon extended beyond the site of inoculation. The large mononuclear cells, however, appeared at about the same time and in equal number in the lesions of both diabetic and non-diabetic animals and showed no morphologic changes. It is concluded that a significant delay and impaired effectiveness of the response by polymorphonuclear leukocytes, a lack of fibroblastic proliferation and an enhanced growth of the fungus lower host resistance to infection with it and are directly consequent on severe alterations in host metabolism.

1960 ◽  
Vol 112 (6) ◽  
pp. 1069-1084 ◽  
Author(s):  
Walter H. Sheldon ◽  
Heinz Bauer

The role of the tissue mast cells in relation to the acute inflammatory reaction to experimental cutaneous mucormycosis was studied histologically in normal rats, in animals whose tissue mast cells had been depleted of their cytoplasmic granules prior to infection by the administration of compound 48/80 and in others in whom acute alloxan diabetes with acidosis had been produced before injection of the fungus. The discharge of the tissue mast cell granules in normal rats occurred within minutes at the site of infection and appeared to initiate the rapid onset of acute inflammation. The degranulation of the tissue mast cells subsided in a short time and the cells reassumed a normal histologic appearance while inflammation progressed with the formation of circumscribed lesions. In animals pretreated with compound 48/80 in which the tissue mast cells contained no granules, the onset of inflammation was briefly delayed, the intensity of the process was somewhat decreased, fibroblastic proliferation was retarded, and the fungus growth in the early lesions was increased. However, the infection did not spread and the lesions were well localized. The tissue mast cells in the diabetic and acidotic rats completely failed to discharge their cytoplasmic granules, the onset and intensity of the acute inflammatory response were markedly delayed and decreased and the infection progressed rapidly with massive fungus growth invading adjacent tissues. A relationship between the discharged tissue mast cell granules and eosinophilic granulocytes was noted since the latter were numerous among the inflammatory cell exudate in normal rats and scarce in the lesions of the diabetic animals. It is concluded that a function of the tissue mast cells in the normal rat is the rapid initiation of acute inflammation at the site of injury and that degranulation of these cells prior to infection somewhat delays the inflammatory response and therefore slightly diminishes host resistance. Furthermore, a severe metabolic disorder such as acute alloxan diabetes with acidosis, inhibits the normal function of the tissue mast cells, delays and decreases inflammation, and in this manner contributes to the greatly increased susceptibility of the host to infection.


Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P65
Author(s):  
J Nakagawa ◽  
N Matsumoto ◽  
K Yamakawa ◽  
T Yamada ◽  
H Matsumoto ◽  
...  

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