Parelaphostrongylus tenuis (also known as meningeal worm or brainworm) is a neurotropic nematode parasite common to white-tailed deer, Odocoileus virginianus, which causes damage to the central nervous system. Moose (Alces alces), elk (Cervus canadensis), caribou (Rangifer tarandus), mule deer (Odocoileus hemionus), and others are also susceptible to the parasite, but are aberrant hosts and are infected in neurological instead of meningeal tissue. The frequency of infection in these species increases dramatically when their ranges overlap high densities of white-tailed deer.
The lifecycle begins in infected meningeal tissues in the central nervous system (CNS) where adult brainworms lay eggs. The eggs are dislodged from the CNS and pass into the lungs, where they hatch. The larvae are then coughed up, swallowed, and proceed through the gastrointestinal tract. Snails and slugs then serve as intermediate hosts, which are later eaten by ungulates, allowing the process to continue. Changes in climate and habitat beginning in the early 1900s have expanded range overlap between white-tailed deer and moose, increasing the frequency of infection within the moose population.
Lifecycle
thumb|White-tailed deer are a common host of P. tenuis.
The lifecycle of P. tenuis is complex and multistaged.
Adults lay eggs on the dura mater (the outer layer of the meninges) of the brain or directly into the bloodstream of an infected host.
Gastropods such as snails and slugs feed upon the mucus coating of the fecal pellets and ingest the larvae. It is quite common in many populations of white-tailed deer, which have built up a strong resistance.
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.
Symptoms/clinical signs
Brainworm affects neurological and behavioral responses. Deer rarely show any external symptoms of P. tenuis 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, llamas, and alpacas. Rarely, it has been seen in cattle and horses as well. Severe neurological damage similar to that of infected moose is shown to occur in these species. It has been shown through experimental infection that Parelaphostrongylus tenuis can produce severe Meningoencephalomyelitis and paralysis of llamas in two months after infection and with the ingestion of as few as six larvae.
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. so detection of adult worms through necropsy is recommended. Diagnosis in moose is conducted with necropsy to detect worms in the brain or spinal cord. Positive PCR results show evidence of P. tenuis infecting equines.
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. 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. Fenbendazole and ivermectin, combined with anti-inflammatory therapy have been used to manage infections in goats.