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Rats given an initial infection with Angiostrongylus cantonensis had moderately elevated phospholipase B activity in the lungs at 8 and 15 days after challenge, and greatly elevated levels were evident at 35, 43, and 49 days. In the brain, the values were elevated at 15 through 35 days. These periods of increased activity in the lungs and brain coincided with the migration patterns of the third stage larvae and the adult worms in this host. The elevated enzyme levels also were were correlated with increased numbers of eosinophils in the bone marrow at 8 and 15 days and again at 36, 43, and 49 days after infection. Similarly infected rats exhibited leukocytosis at 1 through 10 weeks of observation after challenge, and striking eosinophilia at 1, 7, 8, and 9 weeks. Rats reinfected after removal of the worms of the initial infection by thiabendazole treatment showed an anamnestic response characterized by (i) elevated enzyme values in both the lungs and brain at 1 day after reinfection and (ii) eosinophilia in the bone marrow by day 4. These accelerated responses were accompanied by a significant reduction in the worm burden of the rats. The results, which support our hypothesis that inflammation, elevated phospholipase B activity, and reduction in worm burden are causally related, are discussed in light of similar findings reported earlier from our studies with Trichinella spiralis and Nippostrongylus brasiliensis.

After a primary infection with 100 Angiostrongylus cantonensislarvae, infected rats showed elevated phospholipase B activity in meningeal and brain homogenates beginning with the first week and continuing through the first month of infection. The rise in phospholipase B values through the first 4 weeks, with a prolonged peak spanning days 30 to 31, coincided with the invasion and maturation of the parasites in the brain, and the ensuing sharp decline in phospholipase B levels, shown by the readings on day 45, coincided in turn with the known migration of the worms from the brain to the lungs, which begins about 5 weeks after infection. In the meninges, the pattern of enzyme elevation was generally similar to that in the brain samples except that the highest activity was seen earlier at days 8 to 9, followed by a gradual decline by days 30 to 31 and a sharper drop by day 45. Rats challenged with 100 larvae 53 days after the primary infection exhibited an almost immediate rise of phospholipase B activity in both the brain and meninges; the peaks of activity occurred at day 1 for the meninges and day 25 for the brain, and levels above control values were still present at day 50. Comparison of the total enzymatic content of the cerebral tissue and meninges revealed that a remarkably high proportion of the phospholipase B activity was contained in the meninges. The inference that elevated levels of this enzyme in the cerebral tissue of A. cantonensis-infected rats are due to inflammatory reactions within the meningeal envelopes was confirmed by histochemical demonstration of specific sites of enzymatic activity limited to the meninges. It is of interest that 80% of the cells positive for the enzyme were clearly identifiable as eosinophils since an association of bone marrow eosinophilia and high phospholipase B levels in rats infected with A. cantonensiswas shown in our earlier study of rats infected with this parasite.