SERUM TREATMENT OF LOCALIZED PNEUMOCOCCUS INFECTIONS 809 



exudate in the local lesions. The studies of Rowntree, 1 Medigreceanu, 2 

 and Peabody, 3 showing chlorin retention; of Peabody, 4 showing pro- 

 gressive loss in the oxygen-combining power of the hemoglobin, due to 

 the formation of methemoglobin; of Medigreceanu, 5 showing a deficiency 

 of oxydase or lessened power of the tissues to carry on proper oxidation, 

 and of Neufeld and Bold, 6 Rosenow, 7 Cole, 8 Jobling and Strouse, 9 

 indicating the presence of endotoxins within the pneumococci all these 

 support the view that in pneumonia there is well-marked intoxication, 

 and this, in addition to the effects of the local pulmonary consolidation 

 on the heart, respiration, and nervous system, constitute the main fea- 

 tures of the infection. 



. Regarding the mechanism of recovery from pneumonia, there is 

 little definite information. The recent studies of Neufeld, Dochez, and 

 Clough indicate that antibodies are produced at or about the time of the 

 crisis, and that these are probably responsible for the destruction of the 

 bacteria in the circulating blood, and, to a greater extent, in the local 

 lesion. In the resolution of the local lesion it is probable that ferments 

 play an important part. That resolution does not occur earlier may be 

 due to the overbalancing of the leukocytic ferments by the antiferments 

 of the serum, and the lytic ferments become active only when they reach 

 a point of excess over the antiferments, causing a solution of the fibrin, 

 relieving tension, and affording an outlet for the exudate. According 

 to Vaughan, the pneumococci may be considered as furnishing a ferment 

 that brings about the production of a specific antiferment, capable of 

 reacting upon its substratum, the ferment and the new bacterial tissue, 

 and causing its destruction by a process of solution. Pneumococci in 

 the resolving lesion are probably destroyed by leukocidins released 

 through disintegration of leukocytes, by fatty acids, and probably by 

 antibacterial substances in the blood. 



While it is true that immunity does not usually follow an attack of 

 pneumonia, and, indeed, the patient is apparently hypersusceptible, it 

 has been found experimentally that the antibodies are highly specific 

 for the particular organism causing an infection. Reinfection is, there- 

 fore, possible with an organism belonging to another group, and lia- 



1 Bull. Johns Hopkins Hosp., 1908, xix, 367. 2 Jour. Exper. Med., 1911, xiv, 289. 

 3 Jour. Exper. Med., 1913, xvii, 71. 4 Jour. Exper. Med., 1913, xviii, 7. 



6 Jour. Exper. Med., 1914, xix, 309. 



6 Berl. klin. Wochenschr., 1911, xlviii, 1069. 



7 Jour. Infec. Dis., 1911, ix, 190. 8 Jour. Exper. Med., 1912, xvi, 644. 

 9 Jour. Exper. Med., 1913, xviii, 597. 



