1. With properly selected strains of Type II pneumococci, fatal meningitis may be produced by intrathecal infection in dogs.
2. The pathology of the disease differs from that produced by Type I pneumococci, at least with the strains employed.
3. Type II meningitis is characterized by early, very marked reactions, a very heavy fibrin exudation, and a tendency toward the rapid establishment of blocks.
4. Extreme vasodilatation and. hemorrhage are common.
5. The fibrinopurulent exudate tends to involve the walls and perivascular sheaths of deeply penetrating vessels, thereby causing thrombosis.
6. Thrombosis leads to foci of parenchymatous softening which, on subsequent infection, become brain abscesses.
7. The lateral venticles are a "point of election" for the luxuriant growth of pneumococci. Conversely there is evidence that Type II organisms tend somewhat to disappear from other regions, owing either to spontaneous phagocytosis or to filtration into the blood stream. The lateral ventricles, however, continually renew the supply.
8. Hydrocephalus occurs early—sometimes during the 2nd day of the disease.
9. Central myelitis is common and appears early in the disease.
10. Deep nerve cell lesions with necrosis and neuronophagia are encountered. Their pathology suggests a toxic source.
11. In most cases treatment has been impossible owing to severe early reactions, and only as a prophylactic has optochin-serum therapy any real value. It delays death, but has in no instance cured established disease in the dog.
12. Systemic generalization of Type II meningeal infection in the dog occurs, but it is rarely of sufficient extent to modify prognosis.