Eosinophilic meningitis, a syndrome caused by Angiostrongylus cantonensis (the rat lung worm), was first recognized in New Caledonia in 1950, and has since been reported from Hawaii, Tahiti, other Pacific Islands, Indonesia, and Thailand. The human disease has only been reported from the Far East and the Pacific to date, although infected rats have been found in Madagascar, Mauritius, Ceylon, and Sarawak.
The life cycle was described by workers in Australia in 1955 before the importance of the worm as a human pathogen was known. A delicate filiform nematode, 17 to 25 mm. in length, the adult lives in the lungs of rats, and the eggs are coughed up, swallowed, and pass out in the feces as first-stage larvae. Further development occurs in slugs and snails to the third-stage infective larvae. These larvae are ingested by man either while in this intermediate host or after they have been shed by it onto some other article of food, e.g., lettuce.
Crabs and freshwater prawns have also been found to be infected with these meta-strongylid larvae, but probably act as paratenic hosts. The dispersal of the giant African land snail Achatina fulica may have assisted the spread of the infection. When infective larvae are ingested by the rat, they migrate to the brain and reach young adulthood in four weeks. They then migrate to the pulmonary arteries and after two more weeks start laying eggs.
Unfortunately if man accidentally ingests these infective larvae, they migrate to the brain (as in the rat), and there produce the clinical picture of a meningoencephalitis associated with fever, signs of cerebral irritation, mental deficit, and varying degrees of loss of consciousness. Mild blood eosinophilia is present, and lumbar puncture reveals a fluid under increased pressure with increased protein and many eosinophils (from 100 to 3000 per cubic millimeter.) Occasionally patients present with a facial nerve lesion or complaints of diplopia and paresthesia. A complement fixation test using an extract of adult worms as antigen has been developed. The illness usually persists for some weeks or months and then the patient recovers spontaneously.
Young adult worms have been found in the brain and cerebrospinal fluid of man, and experimental infection of monkeys produces a similar syndrome. The pathology of the brain in fatal cases is one of focal areas of softening, the meninges and subarachnoid space being infiltrated with plasma cells, lymphocytes, eosinophils, and neutrophils. There is perivascular cuffing with chronic inflammatory cells in the brain substance. Careful sectioning of the brain is necessary to find the 0.16 to 8 mm. nematodes.
This condition must be differentiated from a variety of other parasitic infections involving the central nervous system. In Thailand cerebral gnathostomiasis and Angiostrongylus infections occur. Cerebral paragonimiasis could be an important differential diagnosis in parts of the Far East. In other situations the syndrome of eosinophilic meningitis could be produced by cysticercosis, hydatid, schistosomiasis, fascioliasis, trichinosis, and possibly strongyloidiasis. Refinements of serologic diagnostic techniques will help in this sometimes difficult clinical problem.
The author has been able to trace no references to treatment with thiabendazole, although this would seem to be the drug to try. Prevention entails education regarding dangerous foods such as raw crabs and prawns and undercooked snails, and making sure that lettuce is free of slugs and snails. Freezing of crustaceans and molluscs at -15° C. for 12 hours has been found to be effective in destroying the infective larvae of A cantonensis.
