Studies on Natural Immunity to Pneumococcus Type Iii

Abstract

Experimental evidence presented in Paper III* indicates that removal and destruction of both rabbit virulent and avirulent strains of Pneumococcus Type III in the normal animal are brought about by the same means, namely, the phagocytic cells of the body, provided the integrity of the capsule becomes impaired. It leaves unanswered, however, the interesting q~aestion as to whether this phagocytosis is "spontaneous," that is, taking place without the intervention o£ a serum component, or whether the adjuvant action of an antibody is essential to the process. The following experiments although they fail to give a complete answer do nevertheless reveal the participation of an antibody reacting with the somatic C carbohydrate of Tillett, Goebel and Avery (1) which not only appears to play a r61e in the phagocytosis of normal animals but is probably responsible for bringing about the non-type specific immunity which Tillett (2)obtained in rabbits vaccinated with R pneumococcus or the smooth form of a heterologous type. Methods and Materials

Fever management in intensive care patients with infections

“…Temperatures in the human physiological febrile range cause direct inhibition of some viral and bacterial organisms such as influenza virus [ 6 ], Streptococcus pneumonia [ 7 ], [ 8 ], and Neisseria meningitides [ 9 ] which can all cause life-threatening illnesses. For influenza, the degree of heat sensitivity appears to be a determinant of virulence, such that strains with a shut-off temperature of ≤38 °C cause mild symptoms, whereas strains with a shut-off temperature of ≥39 °C cause severe symptoms [ 6 ].…”

Fever Management in Intensive Care Patients with Infections

“…Temperatures in the human physiological febrile range cause direct inhibition of some viral and bacterial organisms such as infl uenza virus [6], Streptococcus pneumonia [7], [8], and Neisseria meningitides [9] which can all cause life-threatening illnesses. For infl uenza, the degree of heat sensitivity appears to be a determinant of virulence, such that strains with a shut-off temperature of ≤38 °C cause mild symptoms, whereas strains with a shut-off temperature of ≥39 °C cause severe symptoms [6].…”

A quantitative analysis of the interactions of antipneumococcal antibody and complement in experimental pneumococcal bacteremia.

“…It was also recognized at that time that antibodies could be induced by injection of rabbits with unencapsulated Pn or with pneumococcal cell wall lysates that reacted with the cell walls of all types of Pn (5,6). With few exceptions (6, 7) the evidence from experimental systems using animal models of pneumococcal disease has been that this antibody plays at most a small role in resistance to infection by encapsulated organisms (8). The reasons for these important differences in efficacy between type-specific anticapsular antibody, which were easily shown to be opsonic (9) and these broadly reactive antibodies have not been carefully explored.…”