other deer may be hosts of the second- and third-stage worms. Moose resistance to P. tenuis is much lower than white-tailed deer, which results in a higher mortality rate. Infected deer density, temperature, climate conditions, and length of transmission periods all affect transmission levels. Areas with higher deer populations experience dramatic increases in incidental brainworm larvae consumption. The temperature and climate conditions of summers can regulate gastropod abundance, with hot, dry summers reducing populations and cool, dry summers increasing populations. High or low gastropod populations directly affect the transmission rate of larval worms to new hosts. Hot, dry summers also reduce the survival numbers of first-stage larvae on fecal pellets. Variation of transmission periods is based on the time when snow is absent from the ground. Gastropods are dormant during snow periods, thus first-stage worms cannot be transmitted to additional hosts. So, shorter seasons of snow are met with longer transmission periods of increased potential for transmission through the intermediate vector gastropods. Symptoms/clinical signs Brainworm affects neurological and behavioral responses. Deer rarely show any external symptoms of P. tenius infection due to their high acquired resistance. Moose, however, have low resistance, and may show a number of symptoms. Though infrequent, cases of moose recovering from brainworm infection have been reported. In both deer and moose, symptom severity does not necessarily vary with severity of infection. Infected individuals may not have any external symptoms. Mild symptoms may include slower movements and response time, frequent stumbling, unusually tilted head, and emaciation. Severe symptoms include extreme weakness, lameness, walking in circles, partial or whole blindness, loss of fear for humans, ataxia, and mortality. Several other ungulates are susceptible to brainworm infection, including elk, caribou, mule deer, sheep, goats, alpacas, rarely cattle, and rarely horses. Severe neurological damage similar to that of infected moose is shown to occur in these species. Diagnosis Presently, a commercial antibody test that can detect P. tenuis antemortem does not exist. Diagnosis in deer can be conducted by analyzing fecal pellets for larval P. tenuis, or post mortem necropsy to detect presence of adult P. tenuis in the brain cavity or second- and third-stage worms along the spinal cord. However, brainworm larvae are difficult to distinguish from other parasitic worm species that can also be found in fecal pellets, so detection of adult worms through necropsy is recommended. Diagnosis in moose is conducted with necropsy to detect worms in