Home / Publications / Scientific publications / Scientific Papers 2014 / The reindeer brain worm (Elaphostrongylus rangiferi) – biology and veterinary aspects

The reindeer brain worm (Elaphostrongylus rangiferi) – biology and veterinary aspects

Josefsen TD, Handeland K. Reinens hjernemark (Elaphostrongylus rangiferi) – livssyklus og veterinærmedisinske aspekter. [The reindeer brain worm (Elaphostrongylus rangiferi) – biology and veterinary aspects]. Norsk veterinærtidsskrift 2014; 126(2): 200-206 (In Norwegian with English summary).

The reindeer brain worm (Elaphostrongylus rangiferi) is a widespread and common parasitic nematode with reindeer as final host and gastropods as intermediate hosts. Reindeer shed first stage larvae (L1) in faeces, and L1 develop into infective third stage larvae (L3) in gastropods. Reindeer ingest gastropods with infective L3 during grazing, and L3 are carried by the blood to the brain and spinal cord (CNS). Here, the L3 develop into adult worms, which subsequently migrate into the skeletal muscles. Here they live in reproducing pairs in the muscle fasciae. Gravid females deposit eggs into veins, and the eggs are carried by the  blood stream to the lungs where the L1 hatch. L1 migrate up the airways to the pharynx, then they are swallowed and shed in faeces. The development from L3 to adult in CNS may cause clinical disease in heavily infected animals. Clinical symptoms are ataxia and posterior paresis that may progress to complete paralysis. The disease occurs in late autumn and winter. Calves are most commonly affected. The diagnosis is  based upon clinical signs and season, and can only be verified through thorough post-mortem examination. No effective treatment is known, but slightly affected animals may recover spontaneously.  Elaphostrongylus rangiferi may also infect other ruminants: Clinical disease is not uncommon in goats, occurs sporadically in sheep and has been reported in moose and muskoxen. Clinical signs are similar to those in reindeer. Due to the temperature dependent development from L1 to L3 in gastropods, clinical disease occurs at higher frequency after warm summers.

NVI authors

Josefsen Terje Domaas

Veterinary pathologist (permisjon)

Handeland Kjell

Fagansvarlig vilthelse