(1/935) Human rabies--Virginia, 1998.

On December 31, 1998, a 29-year-old man in Richmond, Virginia, died from rabies encephalitis caused by a rabies virus variant associated with insectivorous bats. This report summarizes the clinical and epidemiologic investigations by the Virginia Department of Health and CDC.  (+info)

(2/935) Human rabies prevention--United States, 1999. Recommendations of the Advisory Committee on Immunization Practices (ACIP).

These revised recommendations of the Advisory Committee on Immunization Practices update the previous recommendations on rabies prevention (MMWR 1991;40[No.RR-3]:1-14) to reflect the current status of rabies and antirabies biologics in the United States. This report includes new information about a human rabies vaccine approved for U.S. use in 1997, recommendations regarding exposure to bats, recommendations regarding an observation period for domestic ferrets, and changes in the local administration of rabies immune globulin.  (+info)

(3/935) Compendium of Animal Rabies Control, 1999. National Association of State Public Health Veterinarians, Inc.

The purpose of this Compendium is to provide information on rabies control to veterinarians, public health officials, and others concerned with rabies control. These recommendations serve as the basis for animal rabies-control programs throughout the United States and facilitate standardization of procedures among jurisdictions, thereby contributing to an effective national rabies-control program. This document is reviewed annually and revised as necessary. Immunization procedure recommendations are contained in Part I; all animal rabies vaccines licensed by the United States Department of Agriculture (USDA) and marketed in the United States are listed in Part II; Part III details the principles of rabies control.  (+info)

(4/935) Mass treatment of humans who drank unpasteurized milk from rabid cows--Massachusetts, 1996-1998.

Rabies is a viral zoonosis that is usually transmitted by the bite of an infected mammal. However, in Massachusetts, two incidents have been reported since 1996 of potential mass exposures to rabies through drinking unpasteurized milk. This report presents the investigations of these two incidents.  (+info)

(5/935) Human rabies postexposure prophylaxis during a raccoon rabies epizootic in New York, 1993 and 1994.

We describe the epidemiology of human rabies postexposure prophylaxis (PEP) in four upstate New York counties during the 1st and 2nd year of a raccoon rabies epizootic. We obtained data from records of 1,173 persons whose rabies PEP was reported to local health departments in 1993 and 1994. Mean annual PEP incidence rates were highest in rural counties, in summer, and in patients 10 to 14 and 35 to 44 years of age. PEP given after bites was primarily associated with unvaccinated dogs and cats, but most (70%) was not attributable to bites. Although pet vaccination and stray animal control, which target direct exposure, remain the cornerstones of human rabies prevention, the risk for rabies by the nonbite route (e. g., raccoon saliva on pet dogs' and cats' fur) should also be considered.  (+info)

(6/935) Risk for rabies transmission from encounters with bats, Colorado, 1977-1996.

To assess the risk for rabies transmission to humans by bats, we analyzed the prevalence of rabies in bats that encountered humans from 1977 to 1996 and characterized the bat-human encounters. Rabies was diagnosed in 685 (15%) of 4,470 bats tested. The prevalence of rabies in bats that bit humans was 2.1 times higher than in bats that did not bite humans. At least a third of the encounters were preventable.  (+info)

(7/935) Modification of membrane currents in mouse neuroblastoma cells following infection with rabies virus.

1. The effect on membrane currents of infection of mouse neuroblastoma NA cells with rabies virus was studied by using the whole-cell patch clamp technique. 2. Three types of membrane currents, namely voltage-dependent Na+ current (I(Na)), delayed rectifier K+ current (I(K-DR)) and inward rectifier K+ current (I(K-IR)) were elicited in uninfected cells. 3. In cells 3 days after infection with the virus, no detectable change was observed in morphology and membrane capacitance, but I(Na) and I(K-IR) were significantly decreased in amplitude without any appreciable difference in the time course of current activation and inactivation. The voltage-dependence of I(Na) activation was significantly shifted in the positive direction along the voltage axis with a decreased slope. I(K-DR) remained almost unaltered after the viral infection. 4. The resting membrane potential, measured with a physiological K+ gradient across the cell membrane, was decreased (depolarized) after the viral infection. The depolarization was associated with the decreased amplitude of I(K-IR). 5. These results suggest that infection of mouse neuroblastoma NA cells with rabies virus causes reduction of functional expression of ion channels responsible for I(Na) and I(K-IR), and provide evidence for possible involvement of the change in membrane properties in the pathogenesis of rabies disease.  (+info)

(8/935) Soluble ectodomain of rabies virus glycoprotein expressed in eukaryotic cells folds in a monomeric conformation that is antigenically distinct from the native state of the complete, membrane-anchored glycoprotein.

Rabies virus glycoprotein (G) is a trimeric type I transmembrane glycoprotein that mediates both virus receptor recognition and low pH-induced membrane fusion. G can assume three different states: the 'native' state (N) detected at the virus surface, which is responsible for receptor binding, the activated hydrophobic state (A), which interacts with the target membrane as a first step in the fusion process, and the fusion-inactive conformation (I). These three states, which are structurally different, are in a pH-dependent equilibrium. This equilibrium is shifted toward the I state at low pH. This paper includes an investigation of the structure of the ectodomain of the PV strain of rabies virus when it is synthesized as a soluble form (G1-439) lacking the transmembrane and intracytoplasmic domains (residues 440-505). It is shown that, whatever the extracellular pH, G1-439 is secreted as a monomer that has the antigenic characteristics of the I state. This I-like state is not acquired in the acidic compartments of the Golgi but directly in the endoplasmic reticulum. Finally, membrane anchorage by the G transmembrane domain (G1-461) is sufficient for the G ectodomain to be folded into the native N form. These results emphasize the role of the G transmembrane domain in the correct folding of the ectodomain.  (+info)