Elaphostrongylus rangiferi was introduced to caribou (Rangifer tarandus caribou) of Newfoundland by infected reindeer (R. t. tarandus) from Norway and has caused at least two epizootics of cerebrospinal elaphostrongylosis (CSE), a debilitating neurologic disease. In an attempt to understand the conditions necessary for such outbreaks, we examined the effects of herd density and climatic factors on parasite abundance. The abundance of E. rangiferi was represented by counts of first-stage larvae in feces collected from young caribou (calves and yearlings) in 7 distinct caribou herds in Newfoundland. Abundance of E. rangiferi was highest in February and in the Avalon (632 ± 14 (mean ± SE)) and St. Anthony (526 ± 145) herds, the 2 herds in which CSE was most frequently reported. Mean abundance in February samples from young animals correlated positively with mean annual minimum temperature (rS = 0.829, df = 6, P = 0.04) and the number of days per year above 0°C (rS = 0.812, df = 6, P = 0.05) and negatively with mean summer temperatures (rS = 0.830, df = 6, P = 0.04). Results suggest that abundance of E. rangiferi and the likelihood of cases of CSE are increased by moderate summer temperatures suitable for the activity and infection of gastropod intermediate hosts and by mild winters with little snow that extend the transmission period. Abundance of larvae was not correlated with herd density. Animals in all 7 herds also had the muscle worm Parelaphostrongylus andersoni, a related nematode with similar dorsal-spined larvae. In 2 additional herds (Cape Shore and Bay de Verde), P. andersoni occurred alone and larvae were passed only by young caribou. In herds with dual infections, numbers of P. andersoni larvae were depressed, declined more quickly in young animals, and were considered to be present in only low numbers in February samples used for E. rangiferi analysis. Upon initial infection, young caribou develop a resistance to E. rangiferi that prevents or reduces reinfection later in life. This was demonstrated by examining the brains of caribou for recently acquired worms, which must develop there for up to 90 days before continuing their tissue migration into the skeletal muscles. Recent infections were detected in only calves and yearlings in all herds with E. rangiferi except the Avalon herd, where developing worms were also found on the brains of older caribou. The infection of older animals in the Avalon herd may reflect a lower immunocompetence of a naive herd that has only recently been exposed to E. rangiferi.
A COMPLEMENT FIXATION TEST FOR POLIOMYELITIS