the brain or spinal cord. Diagnosis in horses can be conducted with postmortem samples used for polymerase chain reaction (PCR) testing. Positive PCR results show evidence of P. tenuis infecting equines. In veterinary patients, such as goats, an eosinophilic pleocytosis can be suggestive of P. tenuis infection. History In 1912, an unknown neurological disease affecting moose was first reported in Minnesota. Major declines in the moose population were reported, 1925–27 and 1933–34, following the discovery of this unknown disease. In 1963, a meningeal brainworm, Pneumostrongylus tenuis, was determined as the etiological agent causing neurological disease in moose. Around 1971, taxonomists reclassified it as Parelaphostrongylus tenuis. White-tailed deer populations in the eastern United States are now known to be commonly infected with meningeal worm. Infection in the southeastern and western United States is less common. This disease has also been found in the Canadian provinces of Ontario, Saskatchewan, Manitoba, and Nova Scotia. The grassland biomes of the United States and Canada apparently act as a barrier to the movement of the disease. Evidence from Canada seems to support this, since the western distribution of meningeal worm has changed little since the 1960s. Epidemiology The geographic ranges of moose and white-tailed deer were historically separate prior to the 20th century. Moose are well adapted to winter survival, whereas deer are not. They could not withstand the harsh winters in these regions of the northeastern United States and the southeastern provinces of Canada. Deer populations began to move into the southern portions of moose range in the early 1900s following changes in climate, logging, mining, forest fires, and increasing human development. High-quality deer habitat associated with these changes has led to dramatic increases in deer abundance in these regions. White-tailed deer are the normal host of the P. tenuis parasite and are immunologically adapted to its presence. Deer and P. tenuis have coadapted in an evolutionary arms race over time. Deer remain largely unaffected by the presence of P. tenuis because of the immunity they have built as a result of coadaptation. The prevalence and infection rate of P. tenuis in deer is density dependent; increased rates of infection by the parasite are the result of higher deer densities. Moose populations on the southern fringes of their range have recently experienced dramatic declines. As deer encroached upon the southern fringes of moose range, they introduced the parasite to a naïve host, the moose.