westnilevirus11

FIFRA - Federal Insecticide, Fungicide and Rodenticide Act is the main federal law which governs the registration, distribution, sale and use of insecticides.

The U.S. Environmental Protection Agency is responsible for its administration

LARVAL INSECTICIDES

Bacillus thurigiensis (Bt)

The EPA originally registered Bt in 1961 and re-registered it in 1998.

Bt is not toxic to birds, dogs, mice, rats and humans. Tests on humans verified its non-toxicity. It does not persist in the digestive tracts of animals that have eaten it; it breaks down rapidly in the environment and is not a threat to groundwater. The EPA has issued no restrictions for its use around bodies of eater.

Toxicity of Bt to birds, freshwater fish, freshwater aquatic invertebrates, estuarine and marine animals, arthropod predators/parasites, honey bees, annelids and mammalian wildlife will be minimal to nonexistent at the label use rates of registered B. thuringiensis active ingredients.

Bti - Bacillus thuringiensis israelensis is a naturally occurring soil bacteria. It contains a microscopic crystal protein that is specific against mosquitoes, black flies and midges.
Once ingested, the crystal protein is activated in the insect's gut which is highly alkaline. The activated protein binds to receptors on cell membranes of the midgut and the cells break apart.

Bti is a bacteria but does not reproduce in the environment.

Bti has a very narrow window of effectiveness against mosquitoes.

Typically mosquito eggs will hatch become larvae (6 to 8 days) before they change to pupae and emerge as adults.

Bti must be ingested by the mosquito larvae. It will degrade within about a week in the water and must be reapplied often.

METHOPRENE

Methoprene is a synthetic insect growth regulator that disrupts the normal development of some insects. It increases the concentration of growth hormone during the fourth larval instar, thereby disrupting hte transformation to a pupa and killing the insect during the pupal stage.

Methoprene kills slowly

Methoprene was registered by the EPA in 1975. It is used for control of ants, flies, lice, moths, beetles, and fleas. It is also used in the production of a number of foods, including meat, milk, eggs, mushrooms, peanuts, rice and cereals.

The EPA has established a tolerance for methoprene in food products, so human exposure to methoprene is more likely to be from food than from mosquito control.

Methoprene has no adverse effects on human health if ingested or inhaled, but may be slightly toxic if absorbed through the skin.

It metabolizes rapidly and completely in mammals and somewhat more slowly in plants. It degrades rapidly in sunlight and soil.

Methoprene has no toxicity to mallards but is moderately toxic to freshwater fish and some freshwater invertebrates, such as CRAYFISH.

Methoprene is potentially harmful to frogs, toads, and salamanders, but low disage rates used in mosquito control should prevent harm to these species.

ADULT MOSQUITO INSECTICIDES

In 2000, New York City has used RESMETHRIN (Scourge)and Westchester County has used SUMITHRIN (Anvil) as adult mosquito insecticides.

Synthetic Pyrethroids
Resmethrin and sumithrin are both type 1 synthetic pyrethroids.
They poison nerve axons.

Although resmethrin and sumithrin have been used for many years, no data have been reported on their toxicity for human beings.

Comprehensive reviews of the synthetic pyrethroids are scheduled for 2002.

Resmethrin has been registered by the EPA since 1971. It is used to control flying and crawling insects in the home, lawn, garden, and at industrial sites.

Resmethrin is a Restricted Use Pesticide (RUP) which is available for use only by certified pesticide applicators or persons under their direct supervision because of its toxicity to fish.

Sumithrin has been registered by the EPA since 1975. It is used as an insecticide and miticide in commercial, industrial, and institutional non-food areas, in homes and gardens, in greenhouses and in pet quarters and on pets. It is also an RUP.

A review article by Hubalek, Z., and Halouzka, J., entitled "West Nile Fever--A Reemerging Mosquito-Borne Viral Disease in Europe" in: Emerging Infectious Diseases 5(5), 1999. Centers for Disease Control provides a comprehensive history of the west nile virus.

Abstract:

West Nile virus was first isolated from the blood of a febrile woman in the West Nile district of Uganda in 1937.

West Nile virus causes sporadic cases and outbreaks of human and equine disease in Europe (western Mediterranean and sourthern Russia in 1962-64, Belarus and Ukraine in the 1970's and 1980's, Romania in 1996-97, Czechland in 1997, and Italy in 1998).

Environmental factors, including human activities, that enhance population densities of vector mosquitoes (heavy rains followed by floods, irrigation, higher than usual temperature, or formation of ecologic niches that enable mass breeding of mosquitoes) could increase the incidence of West Nile fever.

The 1996-97 outbreak in and near Bucharest, Romania, with more than 500 clinical cases and a case-fatality rate approaching 10%, was the largest outbreak of west nile virus.

Arthropod vectors

Mosquitoes, largely bird-feeding species, are the principal vectors of West Nile Virus. The virus has been isolated from 43 mosquito species - predominately of the genus Culex.

Ticks, bird-feeding argasis (soft) or amblyommine (hard) ticks have been implicated in the spread of the virus.

Human symptoms

West nile fever in humans is a febrile, influenza-like illness, characterized by an abrupt onset (incubation period is 3-6 days) of moderate to high fever (3 to 5 days), headache, sore throat, backache, myalgia, arthralgia, fatigue, conjunctivitis, rash spreading from the trunk to the extremities and head, lymphadenopathy, anorexia, nausea, abdominal pain, diarrhea, and respiratory symptoms.

OCCASIONALLY (less than 15% of cases), acute aseptic meningitis or encephalitis (associated with neck stiffness, vomiting, confusion, convulsions) occur.

Lab findings involve a slightly increased sedimentation rate and a mild leukocytosis; cerebrospinal fluid in patients with central nervous system involvement is clear, with elevated protein.

The virus can be recovered from the blood for up to 10 days in immunocompetent febrile patients, as late as 22 to 28 days after infection in immunocompromised patients; peak viremia occurs 4-8 days postinfection.

Recovery is complete and permanent sequelae have not been reported. Most fatal cases have been recorded in patients older than 50 years.

MANY OF THE WEST NILE VIRUS SYMPTOMS HAVE BEEN REPRODUCTED IN VOLUNTEERS WITH UNDERLYING NEOPLASTIC DISEASE WHO HAD BEEN INOCULATED WITH VIRUS TO ACHIEVE PYREXIA AND ONCOLYSIS.

Hundreds of West Nile fever cases have been described in Israel and South Africa.

Dr. Bill would like to point out that this summer 2000, 8 people in Israel have died and 120 more have contracted the disease.

In Southern Israel, 3,300 geese were destroyed at a farm after some of the birds died of the disease.

Other Mammals

Inoculation of sheep with West Nile virus results in fever, abortion in pregnant ewes, in contrast to the asymptomatic infection seen in pigs and dogs.
Rabbits, adult albino rats, and guinea pigs are resistant to West nile virus infection, but lab mice and Syrian hamsters are markedly susceptible.

Birds

Birds usually do not show any symptoms when infected with West Nile Virus. However, natural disease due to the virus has been observed in one pigeon in Egypt, and inoculation of pigeons, chickens, ducks, gulls, and corvids cause occasional encephalitis and death or long-term virus persistence. Chick embryos may be killed by the virus.