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Sami reindeer herders have considerable traditional knowledge about a neurological reindeer disease resembling elaphostrongylosis, but the causative agent was not identified prior to the description of the brainworm Elaphostrongylus rangiferi in Russia in 1958. Elaphostrongylosis was quickly recognised as a serious cause of reindeer morbidity and mortality. The ecology, epidemiology and pathophysiology of the disease were studied in Sweden and Norway during the 1960s and in particular the 1970s to 1990s. In Finland, elaphostrongylosis was not recognised as an important disease for Finnish reindeer husbandry, even though the presence of brainworm infection has been documented. Brainworm has an indirect lifecycle with snail and slug intermediate hosts. The free-living L1 larvae have extremely good freeze tolerance and can survive > 360 days at - 80 °C in water (solid ice). Even though reindeer brainworm is clearly well adapted to the Arctic chill, the lifecycle stages outside the reindeer final host are sped up at warmer environmental temperatures. Arctic summer temperatures are close to the developmental threshold of the parasite in the intermediate gastropod hosts (8-10 °C), and the parasite has typically had a 2-year life cycle. Disease outbreaks generally occur during the winter following the infection of reindeer with infected snails and slugs during the summer and autumn. Warmer summers result in faster development of brainworm larvae in the intermediate hosts. Clinical symptoms have been seen reported as early as August, such as in the outbreak in Trøndelag, Norway in 2018. The reindeer brainworm is also a cause of conflict between reindeer herders and small ruminant farmers, because it can cause severe disease in goats and sheep, which share pasture with reindeer. Many knowledge gaps remain if we wish to successfully predict and mitigate for large-scale outbreaks in a future with a predicted warmer, wetter and wilder climate.

Background: Varestrongylus alces, a lungworm in Eurasian moose from Europe has been considered a junior synonym of Varestrongylus capreoli, in European roe deer, due to a poorly detailed morphological description and the absence of a type-series., Methods: Specimens used in the redescription were collected from lesions in the lungs of Eurasian moose, from Vestby, Norway. Specimens were described based on comparative morphology and integrated approaches. Molecular identification was based on PCR, cloning and sequencing of the ITS-2 region of the nuclear ribosomal DNA. Phylogenetic analysis compared V. alces ITS-2 sequences to these of other Varestrongylus species and other protostrongylids., Results: Varestrongylus alces is resurrected for protostrongylid nematodes of Eurasian moose from Europe. Varestrongylus alces causes firm nodular lesions that are clearly differentiated from the adjacent lung tissue. Histologically, lesions are restricted to the parenchyma with adult, egg and larval parasites surrounded by multinucleated giant cells, macrophages, eosinophilic granulocytes, lymphocytes. The species is valid and distinct from others referred to Varestrongylus, and should be separated from V. capreoli. Morphologically, V. alces can be distinguished from other species by characters in the males that include a distally bifurcated gubernaculum, arched denticulate crura, spicules that are equal in length and relatively short, and a dorsal ray that is elongate and bifurcated. Females have a well-developed provagina, and are very similar to those of V. capreoli. Morphometrics of first-stage larvae largely overlap with those of other Varestrongylus. Sequences of the ITS-2 region strongly support mutual independence of V. alces, V. cf. capreoli, and the yet undescribed species of Varestrongylus from North American ungulates. These three taxa form a well-supported crown-clade as the putative sister of V. alpenae. The association of V. alces and Alces or its ancestors is discussed in light of host and parasite phylogeny and host historical biogeography., Conclusions: Varestrongylus alces is a valid species, and should be considered distinct from V. capreoli. Phylogenetic relationships among Varestrongylus spp. from Eurasia and North America are complex and consistent with faunal assembly involving recurrent events of geographic expansion, host switching and subsequent speciation.

The cardiovascular nematode Angiostrongylus vasorum is spreading in the fox and dog populations of northern Europe. A. vasorum can result in severe clinical manifestations in dogs; therefore, specific diagnosis is crucial for assessing its prevalence. In the present study, faecal samples from foxes and domestic dogs were tested by a new polymerase chain reaction (PCR) targeting the second internal transcribed region of the ribosomal DNA (ITS2) of A. vasorum. Initial isolation of faecal larvae by sieving facilitated the processing of larger sample volumes and allowed for the recovery of dead larvae from frozen samples. The sieve-PCR method enabled the identification of a single larva per 2 g of faecal sample and did not amplify DNA of a range of canine helminths, thus presenting a non-invasive tool for wildlife surveillance and for confirmative diagnosis in dogs.

The first report of Aelurostrongylus falciformis (Schlegel 1933) in Fennoscandian badgers is described. Routine parasitological examination of nine Norwegian badgers, at the National Veterinary Institute during 2004 and 2005, identified A. falciformis in the terminal airways of five of the animals. The first stage larvae (L1) closely resembled, in size and morphology, those of Angiostrongylus vasorum (Baillet 1866). The diagnosis for both A. falciformis and A. vasorum is frequently based on the identification of L1 in faeces or sputum. The potential for misclassification of an A. falciformis infection as A. vasorum, where larval identification is the only diagnostic method used, is discussed.