332 MENINGOCOCCUS^GONOCOCCUS— CATARRH ALIS GROUP 
toxic action of the organism. The "endotoxin" resulting from the 
autolysis of cultures of meningococci is relatively thermostabile; an 
exposure to 100° C. for one-half hour fails to destroy its toxicity. 
Gordon' has described a thermostabile hemolysin, soluble in alco- 
hol, water and acetone, but insoluble in ether. It resists a tempera- 
ture (autoclave) of 120° C. This hemolysin is endocellular, and 
appears in solution in broth cultures of meningococci only when auto- 
lysis is well marked. Hemolysis of blood agar cultures does not appear 
for three to six days. 
Pathogenesis.— The meningococcus possesses but feeble pathogenic 
powers for guinea-pigs; all attempts to induce infection by subcuta- 
neous injections, according to Councilman, Mallory and Wright,^ 
were negative. Occasionally successful results were obtained from 
intraperitoneal and intrapleural inoculation. A slight fibrino-purulent 
exudate was found postmortem in the peritoneal or plevu-al cavities 
in the fatal cases. The adrenals are frequently internally congested. 
Maclagan and Cooke^ have described a similar lesion in the rapidly 
fatal infection in man. Intracranial inoculations were uniformly 
negative. One successful infection of a goat by spinal canal inocu- 
lation was obtained by these observers; the animal died within twenty- 
four hours, and autopsy revealed intense congestion of the meninges 
of the cord and brain. A small amount of purulent spinal fluid was 
obtained containing but little fibrin. Small numbers of cocci were 
found within the polymorphonuclear leukocytes. Flexner* and von 
Lingelsheim and Leuchs'^ have reproduced the essential lesions of 
cerebrospinal meningitis in monkeys by the subdural injection of 
suspensions of the organisms. The organisms were recovered in pure 
culture at autopsy. 
The evidence of the etiological relation of the meningococcus to 
cerebrospinal meningitis in man is essentially the common, almost 
constant demonstration of meningococci in the cerebrospinal fluid; 
frequently from the blood stream, the nasopharynx and exudates 
antemortem; and from the tissues of the brain and cord postmortem. 
It must be remembered that other organisms can produce essentially 
the same lesions, however. The nature and extent of the lesions ob- 
served in fatal cases varies somewhat with the time which elapses 
between the onset of symptoms and death. The rapidly fatal cases 
frequently exliibit intense congestion of the membranes of the cord and 
brain; usually a fibrino-purulent exudate forms, more extensive as a 
rule at the base of the brain but readily demonstrable in the spinal fluid 
obtained by lumbar puncture. According to Westenhofter,'^ there is 
commonly a swelling of the tonsils and pharynx in the early stages of 
1 British Med. Jour., 1918, i, 110. 
2 Loc. cit., p. 76. 
3 Jour. Royal Army Med. Corps, 1917, 29, 228. 
* Loc. cit.; also Centralbl. f. Bakteriol. Orig., 1907, 43, 99. 
5 Klin. Jahrb., 1906, 15, 489. 
6 Berl. med. Gesellsch., May 17, 1905; abst. Centralbl. f. Bakteriol., ref., 1905, 36, 754. 
