West Nile Virus’ Spread Tracked Across United States

Abstracts & Commentary

Sources: Petersen LR, Roehrig JT, Hughes JM. West Nile virus encephalitis. N Engl J Med. 2002;347:1225-1226; Leis AA, et al. A poliomyelitis-like syndrome from West Nile virus infection. N Engl J Med. 2002;347:1279-1280; Glass JD, et al. Poliomyelitis due to West Nile virus. N Engl J Med. 2002;347:1280-1281; Gadoth N, et al. Acute anterior myelitis complicating West Nile fever. Arch Neurol. 1979;36:172-173.

West Nile virus, otherwise called West Nile encephalitis, has slowly become a growing American and Canadian viral disease since its first apparent invasion into the Western Hemisphere in 1999. The virus was first identified in Uganda in 1937 and spread to humans by birds and mosquitoes causing infrequent human cases across Northwest Africa, South Europe, and East Asia. Recently, large epidemic outbreaks have occurred in Romania (1996), Russia (1999), and Israel (2000). Harbored by a mosquito-borne flavivirus, the agent primarily infects birds and calicine mosquitoes, which transfer the virus into humans and horses. In seasonal weather areas such as the United States, the bird-mosquito-bird cycle begins in early spring and steadily generates clinical cases up to their maximum number and geography in late summer. As it evolves in one area, infected birds spread the virus to adjoining areas each year. As the geographical map demonstrates, the first onset sources in the United States appeared in the summer of 1999 in New York, Connecticut, New Jersey, Maryland, and Washington DC. In the first winter following the appearance of the virus in America (1999), John Roehrig and associates of the US Arbo Virus Diseases Branch inspected New York’s sewers and other spots where mosquitoes hibernated. "Was the virus there?" others asked. The answer was yes. The following year (2000), the virus had been carried into 8 more adjacent north and south Atlantic states as shown on the map (see Figure).

During the summer of 2001, Peterson, Roehrig, and Hughes noted that the virus had straddled the shores of both sides of the Mississippi River, expanding all the way up from the Gulf of Mexico to Minnesota. Only 2 of the remaining Eastern states remained not infected. By August 12 of this year, 138 human cases of West Nile virus had been identified in 7 states. Most of these came from Louisiana, Mississippi, and Texas. Thus far, the virus has also been detected in mosquitoes, birds, and horses along with 36 cases in the District of Columbia. Only 6 far-western states have yet escaped evidence of the disease.

Transmission of West Nile virus from mosquitoes is not the only source of transmission into persons. Evidence indicates that person-to-person transmission has occurred after the transplantation of 4 infected body organs from a single donor. Blood products are presently being examined to determine the risk of transfusion of blood or body parts from anyone carrying an unknown active infection.

Peterson et al state that in persons younger than 50 and infected with West Nile virus, only a few may become very sick. Out of every 150 infected individuals 1 will develop meningitis or encephalitis. Out of a cohort of infected patients older than 50 years, however, the disease carries a high risk of neurological damage. Over age 50, fever, muscular weakness, and sometimes delirium become apparent and an accurate diagnosis should be promptly considered. Symptoms may become serious and threatening, and a few patients die.

Of note is the recent identification of poliomyelitis accompanying infection by West Nile virus. It is known that West Nile virus causes poliomyelitis in monkeys, horses, and birds. Gadoth and colleagues identify a young, healthy man of 22 who was tested for clinically apparent positive West Nile encephalitis. Neurologically, along with the acute attack, he developed motor deficits in the face and flaccid paralysis of the left lower extremity with loss of deep-tendon reflexes, but no sensory changes. Within days after onset, the facial paralysis recovered and at 18 months the leg strength had improved, but it remained still "diminished."

Leis et al described 3 male patients, 56, 57, and 50 years old. Two were feverish, 1 was not. All 3 suffered from acute motor paralysis and areflexia, and 2 had bladder dysfunction and acute respiratory distress. Abnormal electrodiagnostic responses identified involvement of either the anterior horn cells or motor axons. Glass and associates described a 50-year-old woman who suffered an acute severe illness characterized by headache, severe myalgia, and severe, sustained general weakness requiring intubation and ventilator support. All 4 patients tested positive for West Nile virus.


This excellent map constructed by Peterson, Roehrig, and Hughes identifies the steady, dynamic invasion and explosive pattern of the spread of West Nile virus in the United States, 1999-2002. Black dots identify the geography of the human disease and density, and the background indicates birds, horses, mosquitoes, and other animals but not humans. Only Arizona, Utah, Nevada, Idaho, Oregon, and Washington remain uninvaded from the disease.

The present reports expand the clinical spectrum of illness attributed to West Nile virus, showing that it can cause a poliomyelitis syndrome with involvement of anterior horn cells. None of the cases were confirmed neuropathologically, but the clinical and electrodiagnostic findings are convincing. Although there is no specific treatment for West Nile virus-induced poliomyelitis, it is important to distinguish these patients from those suffering from Gullian-Barré syndrome to avoid inappropriate treatment. —Fred Plum

Dr. Plum, University Professor, Department of Neurology, Cornell University Medical College, is Editor of Neurology Alert.