This paper demonstrates that the activities of glycogen phosphorylase (GP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are reduced in adult worms of the filarial nematode Litomosoides carinii recovered from pyri-doxine-deficient cotton rats when compared to worms recovered from pyridoxine-sufficient controls. GP, ALT and AST activities were determined in adult worms L. carinii recovered from cotton rat hosts over a 20-week experimental period. Activities of GP, ALT and AST in the parasite showed a direct correlation with the dietary pyridoxine intake of their host. Throughout the experiment, enzyme activities were significantly lower (P < 0·001) in worms from rats fed a pyridoxine-free diet ad libitum that in worms from rats fed either a stock colony diet, a pyridoxine-free diet ad libitum with daily supplementation of 100 μg pyridoxine or limited amounts of pyridoxine-free diet with daily supplementation of 100 μg pyridoxine. The lower than normal activity of GP, ALT, AST and other enzymes dependent on the biologically active derivative of pyridoxine, the coenzyme pyridoxal-5-phosphate (PLP), interferes with the protein, carbohydrate and lipid metabolism of L. carinii and may in part cause the reduced establishment, development and growth of the parasite in pyridoxine-deficient hosts.

Pyridoxine (vitamin B6) deficiency was induced in cotton rats which were then infected with the filarial parasite Litomosoides carinii. Embryogenesis was assessed microscopically in worms taken from pyridoxine deficient cotton rats and from various categories of control animals. Embryogenesis was retarded in worms from pyridoxine deficient hosts and more abnormal embryos were present in such worms than in those from control animals.

Because of the negative binomial distribution of filarial third stage larvae (L3) in their vectors, under natural conditions only a few are usually transferred per bite. After an inoculation of 5 L3 per animal into eight host animals at least one developed a long lasting patency based on one reproductive female only. After an inoculation of 15 L3, three of eight animals developed long lasting patency, harbouring between two and five fertile females. The rates of adult stages recovered were 0·43 and 0·30 respectively. The parasitaemias of the six patent animals in both experimental groups increased with the number of reproductive females present (r=0·89, p=<0·005). All non-patent animals which were mf-negative in the pleural fluid and lung blood as well had a single sex or no worm load. In only one animal was there an apparently normal but non-reproductive pair of worms without any pathological alterations of the host animal. Encapsulated adult worms were found rarely, but independent of the final worm load or inoculation dose and always beside normal adults. In three of the 16 animals inoculated with 5 or 15 L3 patency passed after 10–12 weeks p.i., in two others it seemed to pass soon. After inoculation of 30, 40 or 60 L3 per animal patency passed early in about one half of 105 animals, when they were observed up to 24–36 weeks p.i. In conclusion all types of host defensive reactions are already visible after inoculation with such small doses. Nevertheless even a single inoculation of 5 L3 may give rise to a patent animal and its microfilaraemia is sufficient for transmission under natural conditions. Higher inoculation doses increase the defensive reactions which nevertheless remain unable to destroy all invasive stages.